Ingestion of a greater than optimal quantity of food.
The consumption of edible substances.
A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.
Ventral part of the DIENCEPHALON extending from the region of the OPTIC CHIASM to the caudal border of the MAMMILLARY BODIES and forming the inferior and lateral walls of the THIRD VENTRICLE.
A secreted protein of approximately 131 amino acids that is related to AGOUTI SIGNALING PROTEIN and is also an antagonist of MELANOCORTIN RECEPTOR activity. It is expressed primarily in the HYPOTHALAMUS and the ADRENAL GLAND. As a paracrine signaling molecule, AGRP is known to regulate food intake and body weight. Elevated AGRP has been associated with OBESITY.
A 30-kDa protein synthesized primarily in the ANTERIOR PITUITARY GLAND and the HYPOTHALAMUS. It is also found in the skin and other peripheral tissues. Depending on species and tissues, POMC is cleaved by PROHORMONE CONVERTASES yielding various active peptides including ACTH; BETA-LIPOTROPIN; ENDORPHINS; MELANOCYTE-STIMULATING HORMONES; and others (GAMMA-LPH; CORTICOTROPIN-LIKE INTERMEDIATE LOBE PEPTIDE; N-terminal peptide of POMC or NPP).
An autosomal dominant disorder caused by deletion of the proximal long arm of the paternal chromosome 15 (15q11-q13) or by inheritance of both of the pair of chromosomes 15 from the mother (UNIPARENTAL DISOMY) which are imprinted (GENETIC IMPRINTING) and hence silenced. Clinical manifestations include MENTAL RETARDATION; MUSCULAR HYPOTONIA; HYPERPHAGIA; OBESITY; short stature; HYPOGONADISM; STRABISMUS; and HYPERSOMNOLENCE. (Menkes, Textbook of Child Neurology, 5th ed, p229)
A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.
A nucleus located in the middle hypothalamus in the most ventral part of the third ventricle near the entrance of the infundibular recess. Its small cells are in close contact with the ependyma.
Behavioral responses or sequences associated with eating including modes of feeding, rhythmic patterns of eating, and time intervals.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
A rare condition characterized by recurrent hypersomnias associated with hyperphagia, occurring primarily in males in the second to third decade of life. Clinical features include mental confusion, excessive sleep requirements (approximately 18 hours per day), restlessness, and in some cases hallucinations. Episodes have a duration of days to weeks, and may recur several times per year. This condition may resolve spontaneously over several years. (From Adams, et al., Principles of Neurology, 6th ed, p569)
A melanocortin receptor subtype found primarily in BRAIN. It shows specificity for ALPHA-MSH; BETA-MSH and ADRENOCORTICOTROPIC HORMONE.
Cell surface receptors for obesity factor (LEPTIN), a hormone secreted by the WHITE ADIPOCYTES. Upon leptin-receptor interaction, the signal is mediated through the JAK2/STAT3 pathway to regulate food intake, energy balance and fat storage.
Physiologic mechanisms which regulate or control the appetite and food intake.
Agents that are used to suppress appetite.
Natural recurring desire for food. Alterations may be induced by APPETITE DEPRESSANTS or APPETITE STIMULANTS.
Total number of calories taken in daily whether ingested or by parenteral routes.
Peptide hormones produced by NEURONS of various regions in the HYPOTHALAMUS. They are released into the pituitary portal circulation to stimulate or inhibit PITUITARY GLAND functions. VASOPRESSIN and OXYTOCIN, though produced in the hypothalamus, are not included here for they are transported down the AXONS to the POSTERIOR LOBE OF PITUITARY before being released into the portal circulation.
Agents that are used to stimulate appetite. These drugs are frequently used to treat anorexia associated with cancer and AIDS.
Two populations of Zucker rats have been cited in research--the "fatty" or obese and the lean. The "fatty" rat (Rattus norvegicus) appeared as a spontaneous mutant. The obese condition appears to be due to a single recessive gene.
The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.
Behavioral response associated with the achieving of gratification.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
Area in the hypothalamus bounded medially by the mammillothalamic tract and the anterior column of the FORNIX (BRAIN). The medial edge of the INTERNAL CAPSULE and the subthalamic region form its lateral boundary. It contains the lateral hypothalamic nucleus, tuberomammillary nucleus, lateral tuberal nuclei, and fibers of the MEDIAL FOREBRAIN BUNDLE.
Increase in BODY WEIGHT over existing weight.
Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.
The relative amounts of various components in the body, such as percentage of body fat.
A 28-amino acid, acylated, orexigenic peptide that is a ligand for GROWTH HORMONE SECRETAGOGUE RECEPTORS. Ghrelin is widely expressed but primarily in the stomach in the adults. Ghrelin acts centrally to stimulate growth hormone secretion and food intake, and peripherally to regulate energy homeostasis. Its large precursor protein, known as appetite-regulating hormone or motilin-related peptide, contains ghrelin and obestatin.
An aggregation of cells in the middle hypothalamus dorsal to the ventromedial nucleus and bordering the THIRD VENTRICLE.
A nucleus of the middle hypothalamus, the largest cell group of the tuberal region with small-to-medium size cells.
Nucleus in the anterior part of the HYPOTHALAMUS.
The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.
A serotonin receptor subtype found primarily in the CENTRAL NERVOUS SYSTEM and the CHOROID PLEXUS. This receptor subtype is believed to mediate the anorectic action of SEROTONIN, while selective antagonists of the 5-HT2C receptor appear to induce ANXIETY. Several isoforms of this receptor subtype exist, due to adenine deaminase editing of the receptor mRNA.
Injections into the cerebral ventricles.
A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.
The delivery of a drug into a fluid-filled cavity of the brain.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
A group of disorders characterized by physiological and psychological disturbances in appetite or food intake.
Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.
Hormones secreted by the PITUITARY GLAND including those from the anterior lobe (adenohypophysis), the posterior lobe (neurohypophysis), and the ill-defined intermediate lobe. Structurally, they include small peptides, proteins, and glycoproteins. They are under the regulation of neural signals (NEUROTRANSMITTERS) or neuroendocrine signals (HYPOTHALAMIC HORMONES) from the hypothalamus as well as feedback from their targets such as ADRENAL CORTEX HORMONES; ANDROGENS; ESTROGENS.
Peptides derived from pro-opiomelanocortin (POMC) which can stimulate MELANOCYTES or CORTICOTROPHS. Melanocortins include ACTH; ALPHA-MSH; and other peptides such as BETA-MSH and GAMMA-MSH, derived from other fragments of POMC. These peptides act through a variety of MELANOCORTIN RECEPTORS to control different functions including steroidogenesis, energy homeostasis, feeding, and skin pigmentation.
An imbalanced NUTRITIONAL STATUS resulting from excessive intake of nutrients. Generally, overnutrition generates an energy imbalance between food consumption and energy expenditure leading to disorders such as OBESITY.
A serotonin receptor subtype found in the BRAIN; HEART; LUNGS; PLACENTA and DIGESTIVE SYSTEM organs. A number of functions have been attributed to the action of the 5-HT2B receptor including the development of cardiac myocytes (MYOCYTES, CARDIAC) and the contraction of SMOOTH MUSCLE.
Cell surface receptors that bind CORTICOTROPIN; (ACTH, adrenocorticotropic hormone) with high affinity and trigger intracellular changes. Pharmacology suggests there may be multiple ACTH receptors. An ACTH receptor has been cloned and belongs to a subfamily of G-protein-coupled receptors. In addition to the adrenal cortex, ACTH receptors are found in the brain and immune systems.
The withholding of food in a structured experimental situation.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Cell surface proteins that bind neuropeptide Y with high affinity and trigger intracellular changes which influence the behavior of cells.
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
Full gratification of a need or desire followed by a state of relative insensitivity to that particular need or desire.
The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and SHIVERING are examples of thermogenesis in MAMMALS.
An inbred strain of Long-Evans rats that develops hyperglycemia, hyperinsulinemia, and mild obesity, mostly in males, that resembles non-insulin-dependent diabetes mellitus in humans. It was developed from outbred Long-Evans stock in 1983.
The selection of one food over another.
The processes of heating and cooling that an organism uses to control its temperature.

Role of the CNS melanocortin system in the response to overfeeding. (1/408)

The voluntary suppression of food intake that accompanies involuntary overfeeding is an effective regulatory response to positive energy balance. Because the pro-opiomelanocortin (POMC)-derived melanocortin system in the hypothalamus promotes anorexia and weight loss and is an important mediator of energy regulation, we hypothesized that it may contribute to the hypophagic response to overfeeding. Two groups of rats were overfed to 105 and 116% of control body weight via a gastric catheter. In the first group, in situ hybridization was used to measure POMC gene expression in the rostral arcuate (ARC). Overfeeding increased POMC mRNA in the ARC by 180% relative to levels in control rats. For rats in the second group, the overfeeding was stopped, and they were infused intracerebroventricularly with SHU9119 (SHU), a melanocortin (MC) antagonist at the MC3 and MC4 receptor, or vehicle. Although SHU (0.1 nmol) had no effect on food intake of control rats, intake of overfed rats increased by 265% relative to CSF-treated controls. This complete reversal of regulatory hypophagia not only maintained but actually increased the already elevated weight of overfed rats, whereas CSF-treated overfed rats lost weight. These results indicate that CNS MCs mediate hypophagic signaling in response to involuntary overfeeding and support the hypothesis that MCs are important in the central control of energy homeostasis.  (+info)

Hyperphagia in neonates withdrawing from methadone. (2/408)

AIMS: To examine whether hyperphagia is a clinically significant problem in infants born to women receiving methadone maintenance. METHODS: The volume of feeds, changes in infant body weight, as well as occurrence of adverse clinical effects in infants withdrawing from methadone were studied during the first month of life. A retrospective chart review was conducted for all infants at San Francisco General between 1992 and 1995, born to women receiving methadone maintenance during their pregnancy. Forty four infants were identified and the data obtained from hospital medical records. The daily oral intake of these infants was recorded during the first month of life. The incidence of hyperphagia (oral intake > 190 cc/kg/day) was measured. Associations between infant oral intake and maternal methadone dose were studied using correlation analysis as well as Anova for repeated measures. Adverse clinical symptoms were also recorded. A subset of premature infants was studied separately. RESULTS: The incidence of hyperphagia was 26% by day 8 and 56% by day 16 of life in the infants. Hyperphagia was not associated with maternal methadone dose or with infant withdrawal scores. Infants who were hyperphagic lost significantly more weight during the first week of life than those who were not. Despite significantly greater intake, the hyperphagic infants did not gain weight more rapidly during the first month of life compared with those infants with lower oral intake. Infants who were hyperphagic (maximum intake of 290 cc/kg/day) did not experience increased vomiting, aspiration, diarrhoea, or abdominal distention. CONCLUSIONS: Hyperphagia is commonly found in infants withdrawing from methadone and can be persistent in a significant number. Hyperphagia was not associated with either increased neonatal weight gain or with adverse gastrointestinal consequences. Hyperphagia may occur in infants withdrawing from methadone who have high metabolic demands due to clinical signs not controlled by opiate treatment.  (+info)

Low plasma leptin levels contribute to diabetic hyperphagia in rats. (3/408)

The adipocyte hormone leptin reduces food intake in normal animals. During uncontrolled type 1 diabetes, plasma leptin levels fall, whereas food intake increases. To test the hypothesis that low leptin levels contribute to diabetic hyperphagia, we investigated the effect on food intake of replacement of leptin at basal plasma concentrations for 7 days in Long-Evans rats with uncontrolled diabetes induced by streptozotocin (STZ). One group of STZ diabetic rats received saline (STZ + Sal) (n = 11), while the other group (STZ + Lep) (n = 15) received a subcutaneous infusion of recombinant rat leptin (100 microg x kg(-1) x day(-1)) via osmotic minipumps. A nondiabetic control group (Con) (n = 11) received saline only. In the STZ + Sal group, plasma leptin levels decreased by 75% (P < 0.05) from 2.4+/-0.5 on the day before STZ/citrate buffer vehicle (Veh) injection (day 0) to 0.6+/-0.2 ng/ml on day 7. In contrast, plasma leptin levels on days 3-7 were comparable to pretreatment values in both the STZ + Lep group (day 0: 2.6+/-0.4 vs. day 7: 2.5+/-0.3 ng/ml, NS) and the Con group (day 0: 3.8+/-0.4 vs. day 7: 2.9+/-1.0 ng/ml, NS). In the STZ + Sal group, daily food intake increased gradually to values 43% above basal by day 7 (day 0: 24+/-2 to day 7: 33+/-3 g, P < 0.05), whereas food intake did not increase in either the STZ + Lep group (day 0: 24+/-1 vs. day 7: 21+/-2 g, NS), or the Con group (day 0: 23+/-1 vs. day 7: 23+/-2 g). Plasma glucose levels exceeded nondiabetic control values (7.7+/-0.2 mmol/l) in both diabetic groups, but were lower in the STZ + Lep group (17.2+/-1.8 mmol/l) than in the STZ + Sal group (24.3+/-1.1 mmol/l, P < 0.05). To determine if sensitivity to leptin-induced anorexia was affected by STZ treatment, a second experiment was performed in which the effect of intracerebroventricular leptin injection (at doses of 0.35, 1.0, or 3.5 microg) on food intake was measured 10 days after STZ or Veh treatment. Leptin suppressed both 4- and 24-h food intake in the two groups to an equal extent at every dose (by 15, 22, and 35%, respectively). These findings support the hypothesis that the effect of uncontrolled diabetes to lower leptin levels contributes to diabetic hyperphagia and that this effect is not due to altered leptin sensitivity.  (+info)

Genetically determined obesity in Prader-Willi syndrome: the ethics and legality of treatment. (4/408)

A central characteristic of people with Prader-Willi Syndrome (PWS) is an apparent insatiable appetite leading to severe overeating and the potential for marked obesity and associated serious health problems and premature death. This behaviour may be due to the effects of the genetic defect resulting from the chromosome 15 abnormalities associated with the syndrome. We examine the ethical and legal dilemmas that can arise in the care of people with PWS. A tension exists between a genetic deterministic perspective and that of individual choice. We conclude that the determination of the capacity of a person with PWS to make decisions about his/her eating behaviour and to control that behaviour is of particular importance in resolving this dilemma. If the person is found to lack capacity, the common law principles of acting in a person's "best interests" using the "least restrictive alternative" may be helpful. Allowing serious weight gain in the absence of careful consideration of these issues is an abdication of responsibility.  (+info)

Diazepam-induced hyperphagia in mice is sensitive to quinpirole. (5/408)

The present trial examined the possibility that diazepam (DZP, 1 mg/kg) induces hyperphagia by acting on the dopaminergic system. Quinpirole (QP), dopamine D-2 receptor agonist, was used for this purpose. Mice fasted for 24 hr were treated with QP 1 (QP-1) or 2 (QP-2) mg/kg 30 min prior to termination of the starvation. DZP was given to untreated mice and half of the QP-1 and QP-2 treated mice 10 min before the termination of the starvation. Food consumed during six 30 min intervals (30 min-feeding), food consumed for 3 hr (total feeding), time required to enter the room containing food by passing through a maze with four multiple routes (time to banquet), latent period to commencement of eating food after entering the banquet room (latent period), and feeding frequency for the 30 min intervals as well as for 3 hr were measured. DZP stimulated feeding, shortened the latent period without affecting the time to banquet and increased the feeding frequency. The hyperphagic effect was restricted to the first 30 min interval only. Both QP-1 and QP-2 first reduced, then progressively stimulated, and finally reduced feeding without modifying total feeding, thus making a bell-shaped profile. They also prolonged both the time to banquet and the latent period, and reduced the feeding frequency of the first 30 min interval but not that for 3 hr. Both QP-1 and QP-2 canceled all the effects of DZP. These results imply that dopamine D2 receptor is involved in the induction of hyperphagia by DZP.  (+info)

Hypothalamic orexin expression: modulation by blood glucose and feeding. (6/408)

Orexins (hypocretins), novel peptides expressed in specific neurons of the lateral hypothalamic area (LHA), stimulate feeding when injected intracerebroventricularly. We investigated their role in feeding in the rat by measuring hypothalamic prepro-orexin mRNA levels under contrasting conditions of increased hunger. Prepro-orexin mRNA levels increased significantly after 48 h of fasting (by 90-170%; P < 0.05) and after acute (6 h) hypoglycemia when food was withheld (by 90%; P < 0.02). By contrast, levels were unchanged during chronic food restriction, streptozotocin-induced diabetes, hypoglycemia when food was available, voluntary overconsumption of palatable food, or glucoprivation induced by systemic 2-deoxy-D-glucose. Orexin expression was not obviously related to changes in body weight, insulin, or leptin, but was stimulated under conditions of low plasma glucose in the absence of food. Orexins may participate in the short-term regulation of energy homeostasis by initiating feeding in response to falls in glucose and terminating it after food ingestion. The LHA is known to contain neurons that are stimulated by falls in circulating glucose but inhibited by feeding-related signals from the viscera; orexin neurons may correspond to this neuronal population.  (+info)

Brief periods of hyperphagia cause renal injury in the obese Zucker rat. (7/408)

BACKGROUND: Female obese (fa/fa) Zucker rats are maximally hyperphagic from the beginning of access to solid food until 20 weeks of age and die primarily from renal failure. We documented that urinary albumin excretion (UAE) rises early in obese rats during this time of greatest hyperphagia. This study was conducted to examine if this early surge of hyperphagia is critical to the initiation of glomerular damage. METHODS: Three groups of six-week-old rats were used: (a) obese females fed ad libitum (AL-obese), (b) obese females pair fed to lean controls until 21 weeks and then allowed to eat ad libitum until 57 weeks (PF. AL-obese), (c) lean (Fa/Fa) Zucker rats fed ad libitum (AL-lean). Cohorts of AL-obese and PF.AL-obese rats were allowed to continue to death or 57 weeks of age, and the rest were terminated at 21 weeks for renal histology. RESULTS: At 21 weeks, neither PF.AL-obese nor AL-lean rats had elevated UAE or glomerular histopathology. In contrast, glomerular injury was severe in AL-obese rats. UAE increased by 10 and 29 weeks in AL- and PF.AL-obese rats, respectively. Plasma triglycerides increased prior to UAE in both PF. AL- and AL-obese rats. CONCLUSIONS: In obese rats fed ad libitum, hyperphagia is followed within a few weeks by hypertriglyceridemia and then by glomerular injury regardless of when ad libitum feeding is initiated. These events do not occur in lean rats or in obese rats pair fed to lean rats. Protective effects of pair feeding did not extend into the period of ad libitum feeding for PF.AL-obese rats. Hyperphagia quickly initiates glomerular injury in obese female Zucker rats.  (+info)

Brain-derived neurotrophic factor-deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities. (8/408)

Brain-derived neurotrophic factor (BDNF) has trophic effects on serotonergic (5-HT) neurons in the central nervous system. However, the role of endogenous BDNF in the development and function of these neurons has not been established in vivo because of the early postnatal lethality of BDNF null mice. In the present study, we use heterozygous BDNF(+/-) mice that have a normal life span and show that these animals develop enhanced intermale aggressiveness and hyperphagia accompanied by significant weight gain in early adulthood; these behavioral abnormalities are known to correlate with 5-HT dysfunction. Forebrain 5-HT levels and fiber density in BDNF(+/-) mice are normal at an early age but undergo premature age-associated decrements. However, young adult BDNF(+/-) mice show a blunted c-fos induction by the specific serotonin releaser-uptake inhibitor dexfenfluramine and alterations in the expression of several 5-HT receptors in the cortex, hippocampus, and hypothalamus. The heightened aggressiveness can be ameliorated by the selective serotonin reuptake inhibitor fluoxetine. Our results indicate that endogenous BDNF is critical for the normal development and function of central 5-HT neurons and for the elaboration of behaviors that depend on these nerve cells. Therefore, BDNF(+/-) mice may provide a useful model to study human psychiatric disorders attributed to dysfunction of serotonergic neurons.  (+info)

Hyperphagia is a medical term that describes excessive eating or increased appetite, often to the point of compulsive overeating. It's more than just a simple increase in hunger or appetite; it's characterized by consuming large amounts of food beyond what is needed for normal growth and health.

This condition can be associated with several medical conditions. For instance, it's a common symptom in Prader-Willi syndrome, a genetic disorder that affects appetite, growth, and cognitive development. It can also occur in certain types of brain injuries or disorders affecting the hypothalamus, a part of the brain that regulates hunger and fullness signals.

However, it's important to note that hyperphagia should not be confused with binge eating disorder, another eating disorder characterized by consuming large amounts of food in a short period of time, but without the feeling of loss of control that is typical of binge eating.

As always, if you or someone else is experiencing symptoms of hyperphagia, it's important to seek medical advice to identify and treat any underlying conditions.

The medical definition of "eating" refers to the process of consuming and ingesting food or nutrients into the body. This process typically involves several steps, including:

1. Food preparation: This may involve cleaning, chopping, cooking, or combining ingredients to make them ready for consumption.
2. Ingestion: The act of taking food or nutrients into the mouth and swallowing it.
3. Digestion: Once food is ingested, it travels down the esophagus and enters the stomach, where it is broken down by enzymes and acids to facilitate absorption of nutrients.
4. Absorption: Nutrients are absorbed through the walls of the small intestine and transported to cells throughout the body for use as energy or building blocks for growth and repair.
5. Elimination: Undigested food and waste products are eliminated from the body through the large intestine (colon) and rectum.

Eating is an essential function that provides the body with the nutrients it needs to maintain health, grow, and repair itself. Disorders of eating, such as anorexia nervosa or bulimia nervosa, can have serious consequences for physical and mental health.

Neuropeptide Y (NPY) is a neurotransmitter and neuropeptide that is widely distributed in the central and peripheral nervous systems. It is a member of the pancreatic polypeptide family, which includes peptide YY and pancreatic polypeptide. NPY plays important roles in various physiological functions such as energy balance, feeding behavior, stress response, anxiety, memory, and cardiovascular regulation. It is involved in the modulation of neurotransmitter release, synaptic plasticity, and neural development. NPY is synthesized from a larger precursor protein called prepro-NPY, which is post-translationally processed to generate the mature NPY peptide. The NPY system has been implicated in various pathological conditions such as obesity, depression, anxiety disorders, hypertension, and drug addiction.

The hypothalamus is a small, vital region of the brain that lies just below the thalamus and forms part of the limbic system. It plays a crucial role in many important functions including:

1. Regulation of body temperature, hunger, thirst, fatigue, sleep, and circadian rhythms.
2. Production and regulation of hormones through its connection with the pituitary gland (the hypophysis). It controls the release of various hormones by producing releasing and inhibiting factors that regulate the anterior pituitary's function.
3. Emotional responses, behavior, and memory formation through its connections with the limbic system structures like the amygdala and hippocampus.
4. Autonomic nervous system regulation, which controls involuntary physiological functions such as heart rate, blood pressure, and digestion.
5. Regulation of the immune system by interacting with the autonomic nervous system.

Damage to the hypothalamus can lead to various disorders like diabetes insipidus, growth hormone deficiency, altered temperature regulation, sleep disturbances, and emotional or behavioral changes.

Agouti-related protein (AGRP) is a neuropeptide that functions as an endogenous antagonist of melanocortin receptors, specifically MC3R and MC4R. It is expressed in the hypothalamus and plays a crucial role in regulating energy balance, body weight, and glucose homeostasis. AGRP increases food intake and decreases energy expenditure by inhibiting melanocortin signaling in the hypothalamus. Dysregulation of AGRP has been implicated in various metabolic disorders, including obesity and type 2 diabetes.

Pro-opiomelanocortin (POMC) is a precursor protein that gets cleaved into several biologically active peptides in the body. These peptides include adrenocorticotropic hormone (ACTH), beta-lipotropin, and multiple opioid peptides such as beta-endorphin, met-enkephalin, and leu-enkephalin.

ACTH stimulates the release of cortisol from the adrenal gland, while beta-lipotropin has various metabolic functions. The opioid peptides derived from POMC have pain-relieving (analgesic) and rewarding effects in the brain. Dysregulation of the POMC system has been implicated in several medical conditions, including obesity, addiction, and certain types of hormone deficiencies.

Prader-Willi Syndrome (PWS) is a genetic disorder that affects several parts of the body and is characterized by a range of symptoms including:

1. Developmental delays and intellectual disability.
2. Hypotonia (low muscle tone) at birth, which can lead to feeding difficulties in infancy.
3. Excessive appetite and obesity, typically beginning around age 2, due to a persistent hunger drive and decreased satiety.
4. Behavioral problems such as temper tantrums, stubbornness, and compulsive behaviors.
5. Hormonal imbalances leading to short stature, small hands and feet, incomplete sexual development, and decreased bone density.
6. Distinctive facial features including a thin upper lip, almond-shaped eyes, and a narrowed forehead.
7. Sleep disturbances such as sleep apnea or excessive daytime sleepiness.

PWS is caused by the absence of certain genetic material on chromosome 15, which results in abnormal gene function. It affects both males and females equally and has an estimated incidence of 1 in 10,000 to 30,000 live births. Early diagnosis and management can help improve outcomes for individuals with PWS.

Leptin is a hormone primarily produced and released by adipocytes, which are the fat cells in our body. It plays a crucial role in regulating energy balance and appetite by sending signals to the brain when the body has had enough food. This helps control body weight by suppressing hunger and increasing energy expenditure. Leptin also influences various metabolic processes, including glucose homeostasis, neuroendocrine function, and immune response. Defects in leptin signaling can lead to obesity and other metabolic disorders.

The arcuate nucleus is a part of the hypothalamus in the brain. It is involved in the regulation of various physiological functions, including appetite, satiety, and reproductive hormones. The arcuate nucleus contains two main types of neurons: those that produce neuropeptide Y and agouti-related protein, which stimulate feeding and reduce energy expenditure; and those that produce pro-opiomelanocortin and cocaine-and-amphetamine-regulated transcript, which suppress appetite and increase energy expenditure. These neurons communicate with other parts of the brain to help maintain energy balance and reproductive function.

Feeding behavior refers to the various actions and mechanisms involved in the intake of food and nutrition for the purpose of sustaining life, growth, and health. This complex process encompasses a coordinated series of activities, including:

1. Food selection: The identification, pursuit, and acquisition of appropriate food sources based on sensory cues (smell, taste, appearance) and individual preferences.
2. Preparation: The manipulation and processing of food to make it suitable for consumption, such as chewing, grinding, or chopping.
3. Ingestion: The act of transferring food from the oral cavity into the digestive system through swallowing.
4. Digestion: The mechanical and chemical breakdown of food within the gastrointestinal tract to facilitate nutrient absorption and eliminate waste products.
5. Assimilation: The uptake and utilization of absorbed nutrients by cells and tissues for energy production, growth, repair, and maintenance.
6. Elimination: The removal of undigested material and waste products from the body through defecation.

Feeding behavior is regulated by a complex interplay between neural, hormonal, and psychological factors that help maintain energy balance and ensure adequate nutrient intake. Disruptions in feeding behavior can lead to various medical conditions, such as malnutrition, obesity, eating disorders, and gastrointestinal motility disorders.

Obesity is a complex disease characterized by an excess accumulation of body fat to the extent that it negatively impacts health. It's typically defined using Body Mass Index (BMI), a measure calculated from a person's weight and height. A BMI of 30 or higher is indicative of obesity. However, it's important to note that while BMI can be a useful tool for identifying obesity in populations, it does not directly measure body fat and may not accurately reflect health status in individuals. Other factors such as waist circumference, blood pressure, cholesterol levels, and blood sugar levels should also be considered when assessing health risks associated with weight.

Body weight is the measure of the force exerted on a scale or balance by an object's mass, most commonly expressed in units such as pounds (lb) or kilograms (kg). In the context of medical definitions, body weight typically refers to an individual's total weight, which includes their skeletal muscle, fat, organs, and bodily fluids.

Healthcare professionals often use body weight as a basic indicator of overall health status, as it can provide insights into various aspects of a person's health, such as nutritional status, metabolic function, and risk factors for certain diseases. For example, being significantly underweight or overweight can increase the risk of developing conditions like malnutrition, diabetes, heart disease, and certain types of cancer.

It is important to note that body weight alone may not provide a complete picture of an individual's health, as it does not account for factors such as muscle mass, bone density, or body composition. Therefore, healthcare professionals often use additional measures, such as body mass index (BMI), waist circumference, and blood tests, to assess overall health status more comprehensively.

Energy metabolism is the process by which living organisms produce and consume energy to maintain life. It involves a series of chemical reactions that convert nutrients from food, such as carbohydrates, fats, and proteins, into energy in the form of adenosine triphosphate (ATP).

The process of energy metabolism can be divided into two main categories: catabolism and anabolism. Catabolism is the breakdown of nutrients to release energy, while anabolism is the synthesis of complex molecules from simpler ones using energy.

There are three main stages of energy metabolism: glycolysis, the citric acid cycle (also known as the Krebs cycle), and oxidative phosphorylation. Glycolysis occurs in the cytoplasm of the cell and involves the breakdown of glucose into pyruvate, producing a small amount of ATP and nicotinamide adenine dinucleotide (NADH). The citric acid cycle takes place in the mitochondria and involves the further breakdown of pyruvate to produce more ATP, NADH, and carbon dioxide. Oxidative phosphorylation is the final stage of energy metabolism and occurs in the inner mitochondrial membrane. It involves the transfer of electrons from NADH and other electron carriers to oxygen, which generates a proton gradient across the membrane. This gradient drives the synthesis of ATP, producing the majority of the cell's energy.

Overall, energy metabolism is a complex and essential process that allows organisms to grow, reproduce, and maintain their bodily functions. Disruptions in energy metabolism can lead to various diseases, including diabetes, obesity, and neurodegenerative disorders.

Kleine-Levin Syndrome (KLS) is a rare and complex neurological disorder characterized by recurring episodes of excessive sleep (hypersomnia), often accompanied by cognitive impairment, altered perception, and behavioral changes. These episodes can last for days or even weeks. The exact cause of KLS remains unknown, but it's thought to involve dysfunction in the hypothalamus and/or thalamus regions of the brain. It primarily affects adolescents, with males being more commonly affected than females. Diagnosis is typically made based on clinical symptoms, as there are no specific diagnostic tests for KLS. Treatment usually involves managing individual symptoms and may include stimulant medications to help reduce excessive sleepiness during episodes.

A melanocortin receptor (MCR) is a type of G protein-coupled receptor that binds melanocortin peptides. The melanocortin system plays crucial roles in various biological processes such as pigmentation, energy homeostasis, sexual function, and inflammation.

The melanocortin receptor 4 (MC4R) is one of the five subtypes of MCRs, which is widely expressed in the central nervous system, including the hypothalamus, and some peripheral tissues. MC4R is a key component in the regulation of energy balance, appetite, and body weight. Activation of MC4R by melanocortin peptides, such as α-melanocyte stimulating hormone (α-MSH), leads to decreased food intake and increased energy expenditure, while antagonism or deficiency of MC4R results in obesity.

In summary, the medical definition of 'Receptor, Melanocortin, Type 4' is a G protein-coupled receptor that binds melanocortin peptides and plays a critical role in regulating energy balance, appetite, and body weight.

Leptin receptors are cell surface receptors that bind to and respond to the hormone leptin. These receptors are found in various tissues throughout the body, including the hypothalamus in the brain, which plays a crucial role in regulating energy balance and appetite. Leptin is a hormone produced by adipose (fat) tissue that signals information about the size of fat stores to the brain. When leptin binds to its receptors, it activates signaling pathways that help regulate energy intake and expenditure, body weight, and glucose metabolism.

There are several subtypes of leptin receptors (LEPR), including LEPRa, LEPRb, LEPC, and LEPD. Among these, the LEPRb isoform is the most widely expressed and functionally important form. Mutations in the gene encoding the leptin receptor can lead to obesity, hyperphagia (excessive hunger), and impaired energy metabolism, highlighting the importance of this receptor in maintaining energy balance and overall health.

Appetite regulation refers to the physiological and psychological processes that control and influence the desire to eat food. This complex system involves a variety of hormones, neurotransmitters, and neural pathways that work together to help maintain energy balance and regulate body weight. The hypothalamus in the brain plays a key role in appetite regulation by integrating signals from the digestive system, fat cells, and other organs to adjust feelings of hunger and fullness.

The hormones leptin and ghrelin are also important regulators of appetite. Leptin is released from fat cells and acts on the hypothalamus to suppress appetite and promote weight loss, while ghrelin is produced in the stomach and stimulates appetite and promotes weight gain. Other factors that can influence appetite regulation include stress, emotions, sleep patterns, and cultural influences.

Abnormalities in appetite regulation can contribute to the development of eating disorders such as anorexia nervosa, bulimia nervosa, and binge eating disorder, as well as obesity and other health problems. Understanding the mechanisms of appetite regulation is an important area of research for developing effective treatments for these conditions.

Appetite depressants are medications or substances that reduce or suppress feelings of hunger and appetite. They can be prescribed to treat various medical conditions, such as obesity or binge eating disorder, where weight loss is a recommended treatment goal. Some common appetite depressants include:

1. Phentermine: This medication works by stimulating the release of certain neurotransmitters in the brain that help suppress appetite and increase metabolism. It is often prescribed for short-term use (up to 12 weeks) as part of a comprehensive weight loss plan.

2. Diethylpropion: Similar to phentermine, diethylpropion stimulates the release of neurotransmitters that suppress appetite and increase metabolism. It is also prescribed for short-term use in treating obesity.

3. Naltrexone-bupropion (Contrave): This combination medication helps manage weight by reducing appetite and increasing feelings of fullness. Naltrexone is an opioid antagonist that blocks the rewarding effects of food, while bupropion is an antidepressant that can help reduce cravings for high-calorie foods.

4. Lorcaserin (Belviq): This medication works by selectively activating serotonin receptors in the brain, which helps promote satiety and reduce appetite. It was withdrawn from the US market in 2020 due to concerns about its potential link to an increased risk of cancer.

5. Topiramate (Topamax): Although primarily used as an anticonvulsant, topiramate has also been found to have appetite-suppressing effects. It is often combined with phentermine in a single formulation (Qsymia) for the treatment of obesity.

6. Cannabis: Some studies suggest that cannabinoids, the active compounds in marijuana, may help reduce hunger and promote weight loss by interacting with the endocannabinoid system in the body. However, more research is needed to fully understand its potential as an appetite depressant.

It's important to note that appetite suppressants should only be used under the guidance of a healthcare professional and as part of a comprehensive weight management plan. These medications can have side effects and potential risks, so it's crucial to discuss their use with your doctor before starting any new treatment regimen.

Appetite is the desire to eat or drink something, which is often driven by feelings of hunger or thirst. It is a complex process that involves both physiological and psychological factors. Physiologically, appetite is influenced by the body's need for energy and nutrients, as well as various hormones and neurotransmitters that regulate hunger and satiety signals in the brain. Psychologically, appetite can be affected by emotions, mood, stress levels, and social factors such as the sight or smell of food.

In medical terms, a loss of appetite is often referred to as anorexia, which can be caused by various factors such as illness, medication, infection, or psychological conditions like depression. On the other hand, an excessive or abnormal appetite is known as polyphagia and can be a symptom of certain medical conditions such as diabetes or hyperthyroidism.

It's important to note that while "anorexia" is a medical term used to describe loss of appetite, it should not be confused with the eating disorder anorexia nervosa, which is a serious mental health condition characterized by restrictive eating, distorted body image, and fear of gaining weight.

"Energy intake" is a medical term that refers to the amount of energy or calories consumed through food and drink. It is an important concept in the study of nutrition, metabolism, and energy balance, and is often used in research and clinical settings to assess an individual's dietary habits and health status.

Energy intake is typically measured in kilocalories (kcal) or joules (J), with one kcal equivalent to approximately 4.184 J. The recommended daily energy intake varies depending on factors such as age, sex, weight, height, physical activity level, and overall health status.

It's important to note that excessive energy intake, particularly when combined with a sedentary lifestyle, can lead to weight gain and an increased risk of chronic diseases such as obesity, type 2 diabetes, and cardiovascular disease. On the other hand, inadequate energy intake can lead to malnutrition, decreased immune function, and other health problems. Therefore, it's essential to maintain a balanced energy intake that meets individual nutritional needs while promoting overall health and well-being.

Hypothalamic hormones are a group of hormones that are produced and released by the hypothalamus, a small region at the base of the brain. These hormones play a crucial role in regulating various bodily functions, including temperature, hunger, thirst, sleep, and emotional behavior.

The hypothalamus produces two main types of hormones: releasing hormones and inhibiting hormones. Releasing hormones stimulate the pituitary gland to release its own hormones, while inhibiting hormones prevent the pituitary gland from releasing hormones.

Some examples of hypothalamic hormones include:

* Thyroid-releasing hormone (TRH), which stimulates the release of thyroid-stimulating hormone (TSH) from the pituitary gland.
* Growth hormone-releasing hormone (GHRH) and somatostatin, which regulate the release of growth hormone (GH) from the pituitary gland.
* Gonadotropin-releasing hormone (GnRH), which stimulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland, which in turn regulate reproductive function.
* Corticotropin-releasing hormone (CRH), which stimulates the release of adrenocorticotropic hormone (ACTH) from the pituitary gland, which regulates the stress response.
* Prolactin-inhibiting hormone (PIH) and prolactin-releasing hormone (PRH), which regulate the release of prolactin from the pituitary gland, which is involved in lactation.

Overall, hypothalamic hormones play a critical role in maintaining homeostasis in the body by regulating various physiological processes.

Appetite stimulants are medications or substances that increase the desire to eat or improve appetite. They work by affecting brain chemicals, hormones, or other systems involved in regulating hunger and fullness. Some commonly used appetite stimulants include:

1. Megestrol acetate: a synthetic progestin hormone that is often prescribed for cancer-related weight loss and anorexia. It works by stimulating appetite and promoting weight gain.
2. Dronabinol: a synthetic form of THC, the active ingredient in marijuana. It is approved for treating AIDS-related anorexia and chemotherapy-induced nausea and vomiting. Dronabinol can increase appetite and promote weight gain.
3. Corticosteroids: medications that mimic the effects of hormones produced by the adrenal gland. They can help improve appetite, but their long-term use is associated with significant side effects.
4. Cyproheptadine: an antihistamine medication that can also stimulate appetite. It is sometimes used off-label to treat appetite loss in various conditions, such as cancer or HIV/AIDS.
5. Ghrelin agonists: these are medications that mimic the effects of ghrelin, a hormone produced by the stomach that increases hunger and appetite. Currently, there are no FDA-approved ghrelin agonists for appetite stimulation, but research is ongoing.

It's important to note that while appetite stimulants can help improve food intake in some individuals, they may not be effective for everyone, and their use should be carefully monitored due to potential side effects and interactions with other medications. Always consult a healthcare professional before starting any new medication or supplement.

I'm sorry for any confusion, but "Rats, Zucker" is not a standard medical term or abbreviation in human medicine. It seems to be an incorrect combination of two terms from the field of laboratory animal science.

1. "Rats" are commonly used laboratory animals.
2. "Zucker" is a surname and also refers to a strain of laboratory rats, specifically the Zucker Diabetic Fatty (ZDF) rat, which is a model for studying type 2 diabetes mellitus.

If you have any questions related to human medicine or healthcare, I would be happy to help clarify those for you.

"Adiposity" is a medical term that refers to the condition of having an excessive amount of fat in the body. It is often used to describe obesity or being significantly overweight. Adipose tissue, which is the technical name for body fat, is important for many bodily functions, such as storing energy and insulating the body. However, an excess of adipose tissue can lead to a range of health problems, including heart disease, diabetes, and certain types of cancer.

There are different ways to measure adiposity, including body mass index (BMI), waist circumference, and skinfold thickness. BMI is the most commonly used method and is calculated by dividing a person's weight in kilograms by their height in meters squared. A BMI of 30 or higher is considered obese, while a BMI between 25 and 29.9 is considered overweight. However, it's important to note that BMI may not accurately reflect adiposity in some individuals, such as those with a lot of muscle mass.

In summary, adiposity refers to the condition of having too much body fat, which can increase the risk of various health problems.

Satiety response is a term used in the field of nutrition and physiology to describe the feeling of fullness or satisfaction that follows food consumption. It is a complex process regulated by several factors, including the mechanical and chemical signals generated during digestion, hormonal responses, and psychological factors. The satiety response helps control food intake and energy balance by inhibiting further eating until the body has had enough time to metabolize and absorb the nutrients from the meal.

The satiety response can be influenced by various factors such as the type, volume, and texture of food consumed, as well as individual differences in appetite regulation and metabolism. Understanding the mechanisms underlying the satiety response is important for developing strategies to promote healthy eating behaviors and prevent overeating, which can contribute to obesity and other health problems.

Adipose tissue, also known as fatty tissue, is a type of connective tissue that is composed mainly of adipocytes (fat cells). It is found throughout the body, but is particularly abundant in the abdominal cavity, beneath the skin, and around organs such as the heart and kidneys.

Adipose tissue serves several important functions in the body. One of its primary roles is to store energy in the form of fat, which can be mobilized and used as an energy source during periods of fasting or exercise. Adipose tissue also provides insulation and cushioning for the body, and produces hormones that help regulate metabolism, appetite, and reproductive function.

There are two main types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). WAT is the more common form and is responsible for storing energy as fat. BAT, on the other hand, contains a higher number of mitochondria and is involved in heat production and energy expenditure.

Excessive accumulation of adipose tissue can lead to obesity, which is associated with an increased risk of various health problems such as diabetes, heart disease, and certain types of cancer.

The lateral hypothalamic area (LHA) is a region in the hypothalamus, which is a part of the brain that plays a crucial role in regulating various autonomic functions and maintaining homeostasis. The LHA is located laterally to the third ventricle and contains several neuronal populations that are involved in diverse physiological processes such as feeding behavior, energy balance, sleep-wake regulation, and neuroendocrine function.

Some of the key neurons found in the LHA include orexin/hypocretin neurons, melanin-concentrating hormone (MCH) neurons, and agouti-related protein (AGRP) neurons. These neurons release neurotransmitters and neuropeptides that modulate various physiological functions, including appetite regulation, energy expenditure, and arousal. Dysfunction in the LHA has been implicated in several neurological and psychiatric disorders, such as narcolepsy, obesity, and depression.

Weight gain is defined as an increase in body weight over time, which can be attributed to various factors such as an increase in muscle mass, fat mass, or total body water. It is typically measured in terms of pounds or kilograms and can be intentional or unintentional. Unintentional weight gain may be a cause for concern if it's significant or accompanied by other symptoms, as it could indicate an underlying medical condition such as hypothyroidism, diabetes, or heart disease.

It is important to note that while body mass index (BMI) can be used as a general guideline for weight status, it does not differentiate between muscle mass and fat mass. Therefore, an increase in muscle mass through activities like strength training could result in a higher BMI, but this may not necessarily be indicative of increased health risks associated with excess body fat.

I cannot precisely define "obese mice" from a medical perspective because "obesity" is typically defined for humans and companion animals based on body weight relative to body size. However, I can provide you with relevant information regarding obese mice in a research or laboratory context.

Obesity in mice is often induced by providing them with a high-fat diet (HFD) to promote excessive weight gain and metabolic dysfunction. This allows researchers to study the effects of obesity on various health parameters, such as insulin resistance, inflammation, and cardiovascular function.

In laboratory settings, mice are often considered obese if their body weight is 10-20% higher than the average for their strain, age, and sex. Researchers also use body mass index (BMI) or body fat percentage to determine obesity in mice. For example:

* Body Mass Index (BMI): Mice with a BMI greater than 0.69 g/cm² are considered obese. To calculate BMI, divide the body weight in grams by the square of the nose-to-anus length in centimeters.
* Body Fat Percentage: Obesity can also be determined based on body fat percentage using non-invasive methods like magnetic resonance imaging (MRI) or computed tomography (CT) scans. Mice with more than 45% body fat are generally considered obese.

It is important to note that these thresholds may vary depending on the mouse strain, age, and sex. Researchers should consult relevant literature for their specific experimental setup when defining obesity in mice.

Body composition refers to the relative proportions of different components that make up a person's body, including fat mass, lean muscle mass, bone mass, and total body water. It is an important measure of health and fitness, as changes in body composition can indicate shifts in overall health status. For example, an increase in fat mass and decrease in lean muscle mass can be indicative of poor nutrition, sedentary behavior, or certain medical conditions.

There are several methods for measuring body composition, including:

1. Bioelectrical impedance analysis (BIA): This method uses low-level electrical currents to estimate body fat percentage based on the conductivity of different tissues.
2. Dual-energy X-ray absorptiometry (DXA): This method uses low-dose X-rays to measure bone density and body composition, including lean muscle mass and fat distribution.
3. Hydrostatic weighing: This method involves submerging a person in water and measuring their weight underwater to estimate body density and fat mass.
4. Air displacement plethysmography (ADP): This method uses air displacement to measure body volume and density, which can be used to estimate body composition.

Understanding body composition can help individuals make informed decisions about their health and fitness goals, as well as provide valuable information for healthcare providers in the management of chronic diseases such as obesity, diabetes, and heart disease.

Ghrelin is a hormone primarily produced and released by the stomach with some production in the small intestine, pancreas, and brain. It is often referred to as the "hunger hormone" because it stimulates appetite, promotes food intake, and contributes to the regulation of energy balance.

Ghrelin levels increase before meals and decrease after eating. In addition to its role in regulating appetite and meal initiation, ghrelin also has other functions, such as modulating glucose metabolism, insulin secretion, gastric motility, and cardiovascular function. Its receptor, the growth hormone secretagogue receptor (GHS-R), is found in various tissues throughout the body, indicating its wide range of physiological roles.

The dorsomedial hypothalamic nucleus (DMH) is a collection of neurons located in the dorsomedial region of the hypothalamus, a part of the brain that regulates various autonomic and endocrine functions. The DMH plays a critical role in regulating several physiological processes, including feeding behavior, energy balance, body temperature, and circadian rhythms.

The neurons in the DMH release different neurotransmitters, such as glutamate, GABA, and neuropeptides, that modulate its functions. The DMH receives inputs from various brain regions, including the limbic system, which is involved in emotional processing, and the brainstem, which regulates autonomic functions.

The DMH also projects to several brain areas, such as the paraventricular hypothalamic nucleus (PVN), lateral hypothalamus, and other regions of the brainstem, forming a complex neural network that controls energy balance and feeding behavior. Dysfunction in the DMH has been implicated in various pathological conditions, including obesity, diabetes, and mood disorders.

The ventromedial hypothalamic nucleus (VMN) is a collection of neurons located in the ventromedial region of the hypothalamus, a part of the brain that regulates various autonomic and endocrine functions. The VMN plays an essential role in regulating several physiological processes, including feeding behavior, energy balance, and glucose homeostasis. It contains neurons that are sensitive to changes in nutrient status, such as leptin and insulin levels, and helps to integrate this information with other signals to modulate food intake and energy expenditure. Additionally, the VMN has been implicated in the regulation of various emotional and motivational states, including anxiety, fear, and reward processing.

The Paraventricular Hypothalamic Nucleus (PVN) is a nucleus in the hypothalamus, which is a part of the brain that regulates various autonomic functions and homeostatic processes. The PVN plays a crucial role in the regulation of neuroendocrine and autonomic responses to stress, as well as the control of fluid and electrolyte balance, cardiovascular function, and energy balance.

The PVN is composed of several subdivisions, including the magnocellular and parvocellular divisions. The magnocellular neurons produce and release two neuropeptides, oxytocin and vasopressin (also known as antidiuretic hormone), into the circulation via the posterior pituitary gland. These neuropeptides play important roles in social behavior, reproduction, and fluid balance.

The parvocellular neurons, on the other hand, project to various brain regions and the pituitary gland, where they release neurotransmitters and neuropeptides that regulate the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for the stress response. The PVN also contains neurons that produce corticotropin-releasing hormone (CRH), a key neurotransmitter involved in the regulation of the HPA axis and the stress response.

Overall, the Paraventricular Hypothalamic Nucleus is an essential component of the brain's regulatory systems that help maintain homeostasis and respond to stressors. Dysfunction of the PVN has been implicated in various pathological conditions, including hypertension, obesity, and mood disorders.

Dexfenfluramine is a medication that was previously used as an appetite suppressant for weight loss. It is a stereoisomer (enantiomer) of fenfluramine, which is another appetite suppressant. Dexfenfluramine works by increasing the levels of serotonin in the brain, which helps to reduce appetite and promote weight loss.

However, dexfenfluramine was withdrawn from the market in 1997 due to concerns about its safety. Studies found that long-term use of dexfenfluramine was associated with an increased risk of primary pulmonary hypertension, a rare but serious condition that can lead to heart failure. Additionally, when dexfenfluramine was used in combination with phentermine (a different appetite suppressant), there was an increased risk of valvular heart disease.

Therefore, dexfenfluramine is no longer available for medical use and its prescription is not recommended due to these safety concerns.

A serotonin receptor, specifically the 5-HT2C (5-hydroxytryptamine 2C) receptor, is a type of G protein-coupled receptor found in the central and peripheral nervous systems. These receptors are activated by the neurotransmitter serotonin (also known as 5-hydroxytryptamine or 5-HT) and play crucial roles in various physiological processes, including mood regulation, appetite control, sleep, and memory.

The 5-HT2C receptor is primarily located on postsynaptic neurons and can also be found on presynaptic terminals. When serotonin binds to the 5-HT2C receptor, it triggers a signaling cascade that ultimately influences the electrical activity of the neuron. This receptor has been associated with several neurological and psychiatric conditions, such as depression, anxiety, schizophrenia, and eating disorders.

Pharmacological agents targeting the 5-HT2C receptor have been developed for the treatment of various diseases. For example, some antipsychotic drugs work as antagonists at this receptor to alleviate positive symptoms of schizophrenia. Additionally, agonists at the 5-HT2C receptor have shown potential in treating obesity due to their anorexigenic effects. However, further research is needed to fully understand the therapeutic and side effects of these compounds.

Intraventricular injections are a type of medical procedure where medication is administered directly into the cerebral ventricles of the brain. The cerebral ventricles are fluid-filled spaces within the brain that contain cerebrospinal fluid (CSF). This procedure is typically used to deliver drugs that target conditions affecting the central nervous system, such as infections or tumors.

Intraventricular injections are usually performed using a thin, hollow needle that is inserted through a small hole drilled into the skull. The medication is then injected directly into the ventricles, allowing it to circulate throughout the CSF and reach the brain tissue more efficiently than other routes of administration.

This type of injection is typically reserved for situations where other methods of drug delivery are not effective or feasible. It carries a higher risk of complications, such as bleeding, infection, or damage to surrounding tissues, compared to other routes of administration. Therefore, it is usually performed by trained medical professionals in a controlled clinical setting.

Adipose tissue, brown, also known as brown adipose tissue (BAT), is a type of fat in mammals that plays a crucial role in non-shivering thermogenesis, which is the process of generating heat and maintaining body temperature through the burning of calories. Unlike white adipose tissue, which primarily stores energy in the form of lipids, brown adipose tissue contains numerous mitochondria rich in iron, giving it a brown appearance. These mitochondria contain a protein called uncoupling protein 1 (UCP1), which allows for the efficient conversion of stored energy into heat rather than ATP production.

Brown adipose tissue is typically found in newborns and hibernating animals, but recent studies have shown that adults also possess functional brown adipose tissue, particularly around the neck, shoulders, and spine. The activation of brown adipose tissue has been suggested as a potential strategy for combating obesity and related metabolic disorders due to its ability to burn calories and increase energy expenditure. However, further research is needed to fully understand the mechanisms underlying brown adipose tissue function and its therapeutic potential in treating these conditions.

Intraventricular infusion is a medical procedure where medication or fluid is delivered directly into the cerebral ventricles of the brain through a catheter. The cerebral ventricles are spaces in the brain that contain cerebrospinal fluid (CSF). This method is often used to administer drugs that need to bypass the blood-brain barrier, which can be difficult for certain medications to cross on their own. It is commonly used in the treatment of conditions such as meningitis, encephalitis, and brain tumors.

The process involves surgically implanting a catheter into one of the ventricles, which is then connected to an external or internal pump that delivers the medication or fluid. The infusion can be done continuously over a period of time or intermittently as needed. This method allows for precise control over the amount and rate of drug delivery to the brain, reducing the risk of systemic side effects and increasing the effectiveness of treatment.

However, it's important to note that intraventricular infusions carry risks such as infection, bleeding, and damage to surrounding tissues. Therefore, they are typically reserved for situations where other treatment options have been exhausted or are not effective.

Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.

Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.

Dietary fats, also known as fatty acids, are a major nutrient that the body needs for energy and various functions. They are an essential component of cell membranes and hormones, and they help the body absorb certain vitamins. There are several types of dietary fats:

1. Saturated fats: These are typically solid at room temperature and are found in animal products such as meat, butter, and cheese, as well as tropical oils like coconut and palm oil. Consuming a high amount of saturated fats can raise levels of unhealthy LDL cholesterol and increase the risk of heart disease.
2. Unsaturated fats: These are typically liquid at room temperature and can be further divided into monounsaturated and polyunsaturated fats. Monounsaturated fats, found in foods such as olive oil, avocados, and nuts, can help lower levels of unhealthy LDL cholesterol while maintaining levels of healthy HDL cholesterol. Polyunsaturated fats, found in foods such as fatty fish, flaxseeds, and walnuts, have similar effects on cholesterol levels and also provide essential omega-3 and omega-6 fatty acids that the body cannot produce on its own.
3. Trans fats: These are unsaturated fats that have been chemically modified to be solid at room temperature. They are often found in processed foods such as baked goods, fried foods, and snack foods. Consuming trans fats can raise levels of unhealthy LDL cholesterol and lower levels of healthy HDL cholesterol, increasing the risk of heart disease.

It is recommended to limit intake of saturated and trans fats and to consume more unsaturated fats as part of a healthy diet.

Eating disorders are mental health conditions characterized by significant disturbances in eating behaviors and associated distressing thoughts and emotions. They include several types of disorders, such as anorexia nervosa, bulimia nervosa, binge eating disorder, and other specified feeding or eating disorders (OSFED). These disorders can have serious medical and psychological consequences if left untreated.

Anorexia nervosa is characterized by restrictive eating, low body weight, and an intense fear of gaining weight or becoming fat. Individuals with anorexia may also have a distorted body image and deny the severity of their low body weight.

Bulimia nervosa involves recurrent episodes of binge eating followed by compensatory behaviors such as purging (e.g., self-induced vomiting, misuse of laxatives or diuretics), fasting, or excessive exercise to prevent weight gain.

Binge eating disorder is characterized by recurrent episodes of eating large amounts of food in a short period of time, often to the point of discomfort, accompanied by feelings of loss of control and distress. Unlike bulimia nervosa, individuals with binge eating disorder do not engage in compensatory behaviors to prevent weight gain.

Other specified feeding or eating disorders (OSFED) include atypical anorexia nervosa, subthreshold bulimia nervosa, and subthreshold binge eating disorder, which may have similar symptoms to the above disorders but do not meet all the diagnostic criteria.

Eating disorders can affect people of any age, gender, race, or ethnicity, and they are often associated with other mental health conditions such as depression, anxiety, and obsessive-compulsive disorder. Treatment typically involves a combination of psychological therapy, nutrition counseling, and medical management to address both the physical and psychological aspects of the disorder.

Neuropeptides are small protein-like molecules that are used by neurons to communicate with each other and with other cells in the body. They are produced in the cell body of a neuron, processed from larger precursor proteins, and then transported to the nerve terminal where they are stored in secretory vesicles. When the neuron is stimulated, the vesicles fuse with the cell membrane and release their contents into the extracellular space.

Neuropeptides can act as neurotransmitters or neuromodulators, depending on their target receptors and the duration of their effects. They play important roles in a variety of physiological processes, including pain perception, appetite regulation, stress response, and social behavior. Some neuropeptides also have hormonal functions, such as oxytocin and vasopressin, which are produced in the hypothalamus and released into the bloodstream to regulate reproductive and cardiovascular function, respectively.

There are hundreds of different neuropeptides that have been identified in the nervous system, and many of them have multiple functions and interact with other signaling molecules to modulate neural activity. Dysregulation of neuropeptide systems has been implicated in various neurological and psychiatric disorders, such as chronic pain, addiction, depression, and anxiety.

Pituitary hormones are chemical messengers produced and released by the pituitary gland, a small endocrine gland located at the base of the brain. The pituitary gland is often referred to as the "master gland" because it controls several other endocrine glands and regulates various bodily functions.

There are two main types of pituitary hormones: anterior pituitary hormones and posterior pituitary hormones, which are produced in different parts of the pituitary gland and have distinct functions.

Anterior pituitary hormones include:

1. Growth hormone (GH): regulates growth and metabolism.
2. Thyroid-stimulating hormone (TSH): stimulates the thyroid gland to produce thyroid hormones.
3. Adrenocorticotropic hormone (ACTH): stimulates the adrenal glands to produce cortisol and other steroid hormones.
4. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH): regulate reproductive function in both males and females.
5. Prolactin: stimulates milk production in lactating women.
6. Melanocyte-stimulating hormone (MSH): regulates skin pigmentation and appetite.

Posterior pituitary hormones include:

1. Oxytocin: stimulates uterine contractions during childbirth and milk ejection during lactation.
2. Vasopressin (antidiuretic hormone, ADH): regulates water balance in the body by controlling urine production in the kidneys.

Overall, pituitary hormones play crucial roles in regulating growth, development, metabolism, reproductive function, and various other bodily functions. Abnormalities in pituitary hormone levels can lead to a range of medical conditions, such as dwarfism, acromegaly, Cushing's disease, infertility, and diabetes insipidus.

Melanocortins are a group of peptides that are derived from the post-translational processing of the proopiomelanocortin (POMC) gene. This gene is expressed in various tissues, including the pituitary gland, hypothalamus, and skin. The POMC precursor protein is cleaved into several active peptides, including adrenocorticotropic hormone (ACTH), β-melanocyte stimulating hormone (MSH), γ-MSH, and α-MSH. These melanocortins exert their effects through binding to melanocortin receptors (MCRs), which are G protein-coupled receptors.

The different melanocortins have distinct physiological roles, but they all share some common functions, such as modulating pigmentation, energy homeostasis, and immune responses. For instance, α-MSH and β-MSH bind to MCRs in the skin and increase melanin production, leading to skin tanning. Additionally, α-MSH can act on MCRs in the hypothalamus to regulate appetite and energy expenditure. ACTH, on the other hand, primarily stimulates the release of cortisol from the adrenal gland, but it can also bind to MCRs and influence pigmentation and sexual behavior.

Overall, melanocortins are crucial signaling molecules that play a significant role in various physiological processes, and dysregulation of melanocortin signaling has been implicated in several diseases, including obesity, depression, and skin disorders.

Overnutrition is a state that occurs when an individual consumes food and drinks in quantities that exceed their energy needs, leading to an excessive accumulation of nutrients, particularly macronutrients (carbohydrates, fats, and proteins) and energy. This condition can result in an imbalance between nutrient intake and energy expenditure, which can contribute to the development of various health issues such as obesity, type 2 diabetes, cardiovascular diseases, non-alcoholic fatty liver disease, and certain types of cancer. It is important to note that overnutrition does not only refer to excessive calorie intake but also encompasses the consumption of nutrients in disproportionate amounts, such as an excessively high intake of saturated fats or sugars, which can have detrimental effects on health.

A serotonin receptor, specifically the 5-HT2B receptor, is a type of G protein-coupled receptor (GPCR) that binds to the neurotransmitter serotonin (5-hydroxytryptamine or 5-HT). These receptors are located on the cell membrane of certain cells, including neurons and other cell types in various organs.

The 5-HT2B receptor is involved in a variety of physiological functions, such as regulating mood, appetite, sleep, and sensory perception. In the cardiovascular system, activation of 5-HT2B receptors can lead to the proliferation of cardiac fibroblasts and changes in the extracellular matrix, which may contribute to heart valve abnormalities.

In the central nervous system, 5-HT2B receptors have been implicated in several neurological conditions, including migraine, depression, and schizophrenia. However, their precise roles in these disorders are not yet fully understood.

Pharmacologically targeting 5-HT2B receptors has led to the development of drugs for various indications, such as antimigraine medications (e.g., telcagepant) and potential treatments for heart failure (e.g., mavacamten). However, some 5-HT2B receptor agonists have also been associated with serious side effects, such as valvular heart disease, which has limited their clinical use.

Corticotropin receptors are a type of cell surface receptor that bind to the hormone corticotropin (also known as adrenocorticotropic hormone or ACTH). These receptors are found in various tissues throughout the body, including the adrenal glands.

There are two main types of corticotropin receptors, known as melanocortin receptor 1 (MC1R) and melanocortin receptor 2 (MC2R). MC2R is the primary receptor for corticotropin in the adrenal glands. When corticotropin binds to this receptor, it stimulates the production and release of steroid hormones, such as cortisol, which help regulate metabolism, immune response, and stress response.

Abnormalities in corticotropin receptors have been implicated in several medical conditions, including certain endocrine disorders and skin pigmentation disorders.

Food deprivation is not a medical term per se, but it is used in the field of nutrition and psychology. It generally refers to the deliberate withholding of food for a prolonged period, leading to a state of undernutrition or malnutrition. This can occur due to various reasons such as famine, starvation, anorexia nervosa, or as a result of certain medical treatments or conditions. Prolonged food deprivation can have serious consequences on physical health, including weight loss, muscle wasting, organ damage, and decreased immune function, as well as psychological effects such as depression, anxiety, and cognitive impairment.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Neuropeptide Y (NPY) receptors are a class of G protein-coupled receptors that bind to and are activated by the neuropeptide Y neurotransmitter. NPY is a 36-amino acid peptide that plays important roles in various physiological functions, including appetite regulation, energy homeostasis, anxiety, depression, memory, and cardiovascular function.

There are five different subtypes of NPY receptors, namely Y1, Y2, Y4, Y5, and Y6 (also known as Y6-like). These receptors have distinct tissue distributions and signaling properties. The Y1, Y2, Y4, and Y5 receptors are widely expressed in the central nervous system and peripheral tissues, while the Y6 receptor is primarily found in the brainstem.

The activation of NPY receptors leads to a variety of intracellular signaling pathways, including the inhibition of adenylate cyclase, activation of mitogen-activated protein kinases (MAPKs), and modulation of ion channel activity. Dysregulation of NPY receptor function has been implicated in several diseases, such as obesity, hypertension, anxiety disorders, and neurodegenerative disorders. Therefore, NPY receptors are considered promising targets for the development of therapeutic agents for these conditions.

Corticosterone is a hormone produced by the adrenal gland in many animals, including humans. It is a type of glucocorticoid steroid hormone that plays an important role in the body's response to stress, immune function, metabolism, and regulation of inflammation. Corticosterone helps to regulate the balance of sodium and potassium in the body and also plays a role in the development and functioning of the nervous system. It is the primary glucocorticoid hormone in rodents, while cortisol is the primary glucocorticoid hormone in humans and other primates.

Satiation is a term used in the field of nutrition and physiology, which refers to the feeling of fullness or satisfaction that one experiences after eating food. It is the point at which further consumption of food no longer adds to the sensation of hunger or the desire to eat. This response is influenced by various factors such as the type and amount of food consumed, nutrient composition, energy density, individual appetite regulatory hormones, and gastric distension.

Satiation plays a crucial role in regulating food intake and maintaining energy balance. Understanding the mechanisms underlying satiation can help individuals make healthier food choices and prevent overeating, thereby reducing the risk of obesity and other related health issues.

Thermogenesis is the process of heat production in organisms. In a medical context, it often refers to the generation of body heat by metabolic processes, especially those that increase the rate of metabolism to produce energy and release it as heat. This can be induced by various factors such as cold exposure, certain medications, or by consuming food, particularly foods high in thermogenic nutrients like protein and certain spices. It's also a key component of weight loss strategies, as increasing thermogenesis can help burn more calories.

"Rats, Inbred OLETF" is a specific strain of laboratory rats used in medical research. "OLETF" stands for "Otsuka Long-Evans Tokushima Fatty," which refers to the fact that this strain was developed by crossbreeding and inbreeding Long-Evans rats from the University of Kyoto with local wild rats in Tokushima, Japan, by Otsuka Pharmaceutical Co.

The OLETF rat is a model for studying obesity, type 2 diabetes, and related metabolic disorders. These rats have a genetic mutation that impairs the function of their cholecystokinin-1 (CCK-1) receptors, which are involved in regulating satiety and insulin secretion. As a result, OLETF rats become obese and develop type 2 diabetes as they age.

Inbred strains like the OLETF rat are useful for medical research because they have a consistent genetic background, making it easier to control variables and study the effects of specific genes or interventions. However, it's important to note that results from animal studies may not always translate directly to humans, so further research is needed to confirm any findings.

Food preferences are personal likes or dislikes towards certain types of food or drinks, which can be influenced by various factors such as cultural background, individual experiences, taste, texture, smell, appearance, and psychological factors. Food preferences can also be shaped by dietary habits, nutritional needs, health conditions, and medication requirements. They play a significant role in shaping an individual's dietary choices and overall eating behavior, which can have implications for their nutritional status, growth, development, and long-term health outcomes.

Body temperature regulation, also known as thermoregulation, is the process by which the body maintains its core internal temperature within a narrow range, despite varying external temperatures. This is primarily controlled by the hypothalamus in the brain, which acts as a thermostat and receives input from temperature receptors throughout the body. When the body's temperature rises above or falls below the set point, the hypothalamus initiates responses to bring the temperature back into balance. These responses can include shivering to generate heat, sweating to cool down, vasodilation or vasoconstriction of blood vessels to regulate heat loss, and changes in metabolic rate. Effective body temperature regulation is crucial for maintaining optimal physiological function and overall health.

Hyperphagia occurs when fat deposits need to be built up over the course of a few days or weeks, for example in wintering birds ... In behavioral ecology, hyperphagia is a short-term increase in food intake and metabolization in response to changing ... Mallards may engage in hyperphagia in response to winter floods that temporarily make available more wetlands for foraging, ... "Behavioural compensation reduces energy expenditure during migration hyperphagia in a large bird". Functional Ecology. 26 (4): ...
Gramlich distinguished the overeating responses to these stimuli as homeostatic hyperphagia and hedonic hyperphagia ... Hedonic hunger or hedonic hyperphagia is "the drive to eat to obtain pleasure in the absence of an energy deficit." Particular ... Genetic variability may influence hedonic hyperphagia. Variation in hedonic hunger levels from person to person may be key in ...
1 November 2001). "Ghrelin causes hyperphagia and obesity in rats". Diabetes. 50 (11): 2540-2547. doi:10.2337/DIABETES.50.11. ...
Patients often present with hyperphagia and rapid weight gain. This rapid weight gain is defined as 20-30 pounds over a 6-12 ...
Baird JP, Choe A, Loveland JL, Beck J, Mahoney CE, Lord JS, Grigg LA (March 2009). "Orexin-A hyperphagia: hindbrain ...
In each pair, one rat became obese and exhibited hyperphagia. The weight of the rat with the surgical lesion rose rapidly for a ...
Some WAGR syndrome patients show severe childhood obesity and hyperphagia; the acronym WAGRO (O for obesity) has been used to ...
Klein-Levine- Critchley syndrome: A syndrome of hypersoomnia and hyperphagia. Levine-Critchley syndrome: Acanthocytosis ...
... or hyperphagia is an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating. ... Knocking out vagal nerve receptors has been shown to cause hyperphagia. Changes in hormones associated with the female ... hyperphagia, and developmental delay (OBHD) Pick's disease Prader-Willi syndrome Proopiomelanocortin deficiency Schaaf-yang ... "Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity". Molecular Metabolism. 3 (6): 595- ...
Mice with a mutation in the leptin receptor gene that prevents the activation of STAT3 are obese and exhibit hyperphagia. The ... These eight mutations all cause extreme obesity in infancy, with hyperphagia. A nonsense mutation in the leptin gene that ...
Hypersexuality, hyperphagia, and aggressive outbursts are indicative of disinhibited instinctual drives. Certain psychoactive ...
These biological factors can interact with environmental elements to further trigger hyperphagia. Frequent intermittent ... often resulting in hyperphagia. Those who experience this biologically instigated increase in appetite during times of stress ... as research shows high cortisol reactivity is associated with hyperphagia, an abnormally increased appetite for food, during ... glands naturally secrete larger quantities of glucocorticoids in response to a stressor are more inclined toward hyperphagia. ...
Unlike Kleine-Levin syndrome, hyperphagia and hypersexuality are not reported in people with menstrual-related hypersomnia, but ... The behavioral disturbances can be composed of hyperphagia, irritability, or sexual disinhibition. The cognitive disorders ...
Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, ... Before 2005, hyperphagia and hypersexuality were thought to occur in all cases. That was changed with the guidelines published ... These changes may include disinhibition, sometimes manifested through hypersexuality, hyperphagia or emotional lability, and ...
At the end of the hyperphagia period it can exceed 600 kg. McLellan, B. N.; Reiner, D. (1994), A review of bear evolution (PDF ...
"Altered lipid homeostasis in Drosophila InsP3 receptor mutants leads to obesity and hyperphagia". Disease Models & Mechanisms. ...
People with PWS have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and ... is Associated with Hyperphagia, Obesity and Hypogonadism". Hum. Mol. Genet. 18 (17): 3257-65. doi:10.1093/hmg/ddp263. PMC ... hyperphagia and obesity, short stature, and behavioral and psychiatric disturbances. The following features and signs are ... deletion causes growth deficiency and hyperphagia in mice". PLOS ONE. 3 (3): e1709. Bibcode:2008PLoSO...3.1709D. doi:10.1371/ ...
June 2009). "A deletion of the HBII-85 class of small nucleolar RNAs (snoRNAs) is associated with hyperphagia, obesity and ... Mouse models of PWS show similar symptoms to humans (hyperphagia and growth deficiency), providing further evidence that PWS is ... 2008). Akbarian S (ed.). "SnoRNA Snord116 (Pwcr1/MBII-85) Deletion Causes Growth Deficiency and Hyperphagia in Mice". PLOS ONE ...
Knocking out vagal nerve receptors has been shown to cause hyperphagia (greatly increased food intake). Parasympathetic ... "Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity". Molecular Metabolism. 3 (6): 595- ...
June 2009). "A Deletion of the HBII-85 Class of Small Nucleolar RNAs (snoRNAs) is Associated with Hyperphagia, Obesity and ... deletion causes growth deficiency and hyperphagia in mice". PLOS ONE. 3 (3): e1709. Bibcode:2008PLoSO...3.1709D. doi:10.1371/ ...
Feeding behaviors in children with ONH often include hyperphagia (overeating), resulting in obesity; or hypophagia (reduced ...
... deletion causes growth deficiency and hyperphagia in mice". PLOS ONE. 3 (3): e1709. Bibcode:2008PLoSO...3.1709D. doi:10.1371/ ...
In Klüver-Bucy syndrome, an individual will display placidity, hyperorality, hypersexuality, and hyperphagia. This condition ...
... deletion causes growth deficiency and hyperphagia in mice". PLOS ONE. 3 (3): e1709. Bibcode:2008PLoSO...3.1709D. doi:10.1371/ ...
Likewise, hyperphagia (excessive eating) may be a result of hormonal imbalances, mental disorders (e.g., depression) and others ... Decreased desire to eat is termed anorexia, while polyphagia (or "hyperphagia") is increased eating. Dysregulation of appetite ...
During the autumn hyperphagia, feeding becomes virtually the full-time task of American black bears. Hard masts become the most ... These bears often eat crops, especially during autumn hyperphagia when natural foods are scarce. Favored crops include apples, ...
The obesity and hyperphagia may be mediated by impaired melanocortin activation of PVN neurons and oxytocin deficiency in these ... Additionally, studies in mice have shown that haploinsufficiency of Sim1 causes obesity that is due to hyperphagia and do not ... Overexpression of SIM1 protects against diet induced obesity and rescues the hyperphagia of agouti yellow mice, who have ... It has been demonstrated that modulating SIM1 levels postnatally also leads to hyperphagia and obesity, suggesting a ...
Kennett GA, Ainsworth K, Trail B, Blackburn TP (February 1997). "BW 723C86, a 5-HT2B receptor agonist, causes hyperphagia and ...
Dörr described this pathology with the name "Secondary hyperphagia and vomiting syndrome in young women", in an article ... Doerr‐Zegers, Otto (1994). "About a particular type of oral perversion in the female: Hyperphagia followed by vomiting". ... "Secondary hyperphagia and vomiting syndrome in young women" in the Chilean Journal of Neuropsychiatry in 1972, an article that ...
This has also been termed "placidity" or "tameness". Dietary changes and hyperphagia, characterized by eating inappropriate ...
Hyperphagia occurs when fat deposits need to be built up over the course of a few days or weeks, for example in wintering birds ... In behavioral ecology, hyperphagia is a short-term increase in food intake and metabolization in response to changing ... Mallards may engage in hyperphagia in response to winter floods that temporarily make available more wetlands for foraging, ... "Behavioural compensation reduces energy expenditure during migration hyperphagia in a large bird". Functional Ecology. 26 (4): ...
Gurney, William S. C. and Nisbet, Roger M. (2004) Resource allocation, hyperphagia and compensatory growth. Bulletin of ... hyperphagia, mathematics, statistics, biology, Probabilities. Mathematical statistics, Biology, Agricultural and Biological ... We found that, although hyperphagia always produces growth compensation, overcompensation additionally requires protein ... which we extend to include hyperphagia. This formulation assumes that the rate of allocation to reserves is controlled by ...
Hyperphagia means youre excessively hungry or youre hungry all the time. It happens sometimes. Its not as uncommon as you ... Hyperphagia in Action: 10 Causes of Excessive Hunger. Wellness / October 5, 2023 October 5, 2023 ...
8 Spooky Parallels Between COVID-19 and Ataxic Hyperphagia. Ataxic Hyperphagia is the fictional zombie pathogen featured in my ... Before I came up with the name Ataxic Hyperphagia, a fifth grader came up with the name Stink Pox. That kid rightly intuited ... In Survivor Max, Ataxic Hyperphagia attacks the brain. Thats how you make a zombie, after all. But CV19 is coming for our ... Similarly, in Survivor Max, it isnt the bite, or the death of the host that activates the Ataxic Hyperphagia (although they ...
Orexin-A hyperphagia: Hindbrain participation in consummatory feeding responses. Endocrinology 2008; 150(3): 1202-1216. ...
Preventing hyperphagia by calorie restriction or pair-feeding averts the health costs of a high-BCAA diet. Our data highlight a ... Increasing the ratio of BCAAs to these amino acids results in hyperphagia and is associated with central serotonin depletion. ... show that, rather than having a direct toxic effect, dietary branched-chain amino acids (BCAAs) appear to induce hyperphagia, ... health costs of chronic high BCAA intakes need not be due to intrinsic toxicity but instead are a consequence of hyperphagia ...
Ibility that CBG induces hyperphagia by means of indirect andor CB1R-independent mechanisms warrants urgent additional ... Ibility that CBG induces hyperphagia by means of indirect andor CB1R-independent mechanisms warrants urgent additional ... Ibility that CBG induces hyperphagia by means of indirect andor CB1R-independent mechanisms warrants urgent additional ... Ibility that CBG induces hyperphagia by means of indirect andor CB1R-independent mechanisms warrants urgent additional ...
hyperphagia (extreme hunger or eating). *hoarding. *hallucinations. *delusions. Treatment for major neurocognitive disorder is ...
... anorexia or hyperphagia), disinhibited behavior (such as hypersexuality). ...
This condition is known as polyphagia or hyperphagia.. 5. Slow-healing sores. Sores or infections that are resistant to healing ...
RFamide peptide QRFP43 causes obesity with hyperphagia and reduced thermogenesis in mice. Endocrinology 147, 2916-2922 (2006). ...
hyperphagia. eating too much hyperpyrexia. excessive body temperature hypertrichologist. person who treats unsightly facial ...
The extreme hunger leads to chronic excessive eating (hyperphagia) and obesity. Beginning in early childhood, affected ...
7 Mutation Induced Hyperphagia * 8 Monumental Bacterial Conglomerate Monolithic slamming brutality from the depths of Russia ...
While ICV injection of NPY into the PVN causes hyperphagia and obesity [174], destruction of the PVN causes hyperphagia and ... MC4R knock-out mice have hyperphagia and obesity [167]. MC3R-deficient mice also have increased fat mass and reduced lean body ... DMN lesions cause hyperphagia and obesity, which suggests a suppressive role in appetite [185]. In diet-induced mice, an ... and leptin-deficient ob/ob mice exhibit hyperphagia and obesity, which can be reversed by leptin administration [157]. ...
This is a process known as hyperphagia. Female black bears(Ursus americanus), go through gestation while hibernating. The young ...
Anorexia and Hyperphagia Produced by Five Pharmacologic Classes of Hal... Pharmacology, Bioche.... 1982. ...
Its Hyperphagia Season at Minnesotas Vince Shute Wildlife Sanctuary. Dust, winds and waters. Bears and people. All swirl ... Biologists call late summer hyperphagia season, the time when black bears go into an overeating frenzy to build up their fat ... Biologists call late summer hyperphagia season, the time when black bears go into an overeating frenzy to build up their fat ...
2005) Central relaxin-3 administration causes hyperphagia in male Wistar rats. Endocrinology 146:3295-3300. doi:10.1210/en.2004 ... The first reported effect of central administration of RLN3 was hyperphagia in satiated, male rats (McGowan et al., 2005). ... Intracerebroventricular administration of RLN3 caused stronger hyperphagia in female than in male rats, and when delivered ...
The same kind of misunderstanding surrounds the controversy which periodically rages over the relative values of white bread and bread made from whole-wheat flour. Both are excellent foods though neither is a complete food; and since man requires a certain amount of suitable protein, of mineral salts and of vitamins as well as of carbohydrates, the superiority of the one bread over the other, as the staple article of diet, lies in the extent to which it excels as a source of these essentials. Seeing, therefore, that white bread is notably more deficient in suitable protein, in vitamins (A, B and E) and in certain essential salts than bread made from whole-wheat flour or, indeed, than any other single food entering into the dietaries of western peoples (with the exception of sugars, starches, and fats which are marketed in the pure state) (McCollum), it is by this much the poorer foundation upon which to build a well-balanced diet. Those who can afford to build upon it, and who possess the ...
This blog is a compilation of my opinions. Its not advice; its information that you can take or leave as you please. I dont intend it to replace professional medical consultation or treatment. Your health is in your own hands ...
experience hyperphagia, or excessive eating, caused by an extreme unsatisfied drive to consume food; ...
These mice exhibit hyperphagia, hyperglycemia, NIDDM and are moderately obese compared to the ICR control line. mRNA was ...
Ghrelin causes hyperphagia and obesity in rats Diabetes Projection of diabetes burden through 2050 Diabetes Care ...
Her obesity was ascribed to hyperphagia and lacking the feeling of satiety. Her social interaction was adequate. She was subtly ...
The process is called hyperphagia.. "During spring and summer, bears eat around 5,000 calories a day, but in the fall, they are ...
Study Title: Investigating A Novel Peptide to Treat Hyperphagia in Children with Prader-Willi Syndrome ...
Supports prader-willi symptom research, such as hyperphagia.. Read More Read More ...
  • Here, we show that when dietary BCAAs are varied against a fixed, isocaloric macronutrient background, long-term exposure to high BCAA diets leads to hyperphagia, obesity and reduced lifespan. (nature.com)
  • Fig. 1: Dietary BCAA imbalance drives hyperphagia and obesity, and shortens lifespan. (nature.com)
  • The extreme hunger leads to chronic excessive eating (hyperphagia) and obesity. (medlineplus.gov)
  • Overeating (hyperphagia) and sedentary behavior are known risk factors for obesity, but research in these areas - especially overeating - has been studied almost exclusively in males. (news-medical.net)
  • Leptin receptor (LEPR) gene mutation is an extremely rare endocrine disease characterized by early-onset obesity, hyperphagia in addition to pituitary hormone deficiency, and metabolic abnormalities. (termedia.pl)
  • [ 4 ] Loss of function of the BDNF gene in some patients with WAGR syndrome may produce obesity and hyperphagia. (medscape.com)
  • It is considered the primary genetic cause of obesity, since it is characterized by hyperphagia. (bvsalud.org)
  • Case report: A boy aged 10 years-old, leucoderma, attended the Discipline of Dentistry for Special Care Patients, Pontifical Catholic University of Paraná (PUCPR), with all the inherent PWS characteristics such as hyperphagia and obesity. (bvsalud.org)
  • Conclusion: Considering the information obtained, it was concluded that the motivation to maintain oral health should be constant for this patient and involve family, since hyperphagia, which is a determinant for obesity, decisively contributes to the evolution of oral diseases. (bvsalud.org)
  • Compensatory hyperphagia after fasting tracks recovery of liver energy status. (bvsalud.org)
  • These mice exhibit hyperphagia, hyperglycemia, NIDDM and are moderately obese compared to the ICR control line. (usda.gov)
  • inhibition of this pathway leads to hyperphagia [overeating] and hyperglycemia," Allen-Rhoades explains. (aacrjournals.org)
  • This condition is known as polyphagia or hyperphagia. (healthline.com)
  • The terms "hyperphagia" and "polyphagia" refer to someone who is focused only on eating, or who eats a large amount before feeling full. (adam.com)
  • Because such diet-induced hyperphagia has been studied primarily in sedentary male rats, the researchers' goal was to investigate the effects of gender and exercise on caloric intake of a diet (chow supplemented with a supply of liquid sweetened condensed milk), chosen for its ability to stimulate hyperphagia. (news-medical.net)
  • In active males, diet-induced hyperphagia was abolished and caloric intake was reduced to that observed during chow feeding. (news-medical.net)
  • In active female rats, diet-induced hyperphagia was attenuated, but not abolished, and caloric intake of the chow plus milk diet remained greater than that observed during chow feeding. (news-medical.net)
  • Prolonged high-fat diet (HFD) exposure is associated with hyperphagia, excess caloric intake and weight gain. (neurosciencenews.com)
  • After initial exposure to a HFD, a brief (24-48 h) period of hyperphagia is followed by the regulation of caloric intake and restoration of energy balance within an acute (3-5 day) period. (neurosciencenews.com)
  • The Kleine-Levin syndrome causes episodic hypersomnia (excessive daytime sleepiness) and hyperphagia. (msdmanuals.com)
  • Fig. 3: Hyperphagia in BCAA200 mice is linked to Trp-mediated serotonin (5-HT) depletion. (nature.com)
  • The mice began eating like crazy-hyperphagia," says Huang. (yale.edu)
  • This led to another publication , in which Huang and Horvath teams used CRISPR knockdown of TET3 specifically in AgRP neurons in mice and discovered this induced hyperphagia as well as anti-anxiety and anti-depressive effects. (yale.edu)
  • In behavioral ecology, hyperphagia is a short-term increase in food intake and metabolization in response to changing environmental conditions. (wikipedia.org)
  • Mallards may engage in hyperphagia in response to winter floods that temporarily make available more wetlands for foraging, heavily increasing their daily food intake to make use of the additional food. (wikipedia.org)
  • Fig. 7: Preventing hyperphagia on high BCAA diets averts metabolic and lifespan costs. (nature.com)
  • It helps to increase appetite and might also induce hyperphagia. (novalabgroup.in)
  • We found that, although hyperphagia always produces growth compensation, overcompensation additionally requires protein allocation control which routes assimilate preferentially to structure during recovery. (strath.ac.uk)
  • He presented to us with rapid weight gain from 2 months of age along with hyperphagia. (termedia.pl)
  • Hyperphagia means you're excessively hungry or you're hungry all the time. (serendipitymommy.com)
  • Ibility that CBG induces hyperphagia by means of indirect andor CB1R-independent mechanisms warrants urgent additional investigation, as this pCB might represent a precious novel therapeutic solution for such applications. (icbinhibitor.com)
  • Biologists call late summer hyperphagia season, the time when black bears go into an overeating frenzy to build up their fat reserves before hibernating for the winter. (northernwilds.com)
  • The researchers' conclude that female rats are more vulnerable than male rats to this "sweet" form of diet-induced hyperphagia. (news-medical.net)
  • This diet-induced hyperphagia was significantly greater in sedentary females (35.7 ± 3.1% increase), relative to sedentary males (9.1 ± 2.2% increase). (news-medical.net)
  • These ghrelin effects were dose dependent, occurred independently from ghrelin-induced hyperphagia, and seemed to be mediated by the sympathetic nervous system. (jci.org)
  • We compare the properties of our dynamic energy budget model with an earlier proposal, due to Kooijman, which we extend to include hyperphagia. (strath.ac.uk)
  • Our data highlight a role for amino acid quality in energy balance and show that health costs of chronic high BCAA intakes need not be due to intrinsic toxicity but instead are a consequence of hyperphagia driven by amino acid imbalance. (nature.com)
  • Preventing hyperphagia by calorie restriction or pair-feeding averts the health costs of a high-BCAA diet. (nature.com)
  • In a state of hyperphagia, bears take advantage of salmon as they stage to lay the next generation. (catchmagazine.net)
  • Nutritional status can alter the expression of these appetite-regulating peptides, but most studies have investigated acute changes with fasting, and the effects of a long-term state of hyperphagia as gestation remains to be fully defined. (europa.eu)
  • They present with features of monosomy 1p36, including developmental delay and mental retardation, dysmorphic features, hypotonia, behavioral abnormalities including hyperphagia, and seizures. (nih.gov)
  • Affected children feel extremely hungry and become obese because of consistent overeating (hyperphagia). (cdc.gov)
  • As expected, the WD mice rapidly gained body weight and became obese, and displayed hyperphagia-a condition characterised by a huge desire for food resulting in excessive food intake. (foodnavigator.com)
  • This syndrome consists of morning anorexia and hyperphagia in the evening, and the children are characteristically obese. (news-medical.net)
  • Hepatic lipid accumulation is a hallmark of type II diabetes (T2D) associated with hyperinsulinemia, insulin resistance, and hyperphagia. (nih.gov)
  • Anorexia and Hyperphagia Produced by Five Pharmacologic Classes of Hal. (erowid.org)
  • Parents of children ages 4-17 years also completed a hyperphagia questionnaire. (nih.gov)
  • Hyperphagia occurs when fat deposits need to be built up over the course of a few days or weeks, for example in wintering birds that are preparing to start on their spring migration, or when feeding habitat conditions improve for only a short duration. (wikipedia.org)
  • Hyperphagia is a feeding frenzy that occurs in the fall prior to hibernation. (americanbear.org)
  • Studies assessing hyperphagia and the leptin pathway have not been previously reported in patients with AS. (nih.gov)
  • The Phase 2 study of RGH-706 will evaluate the efficacy, safety, and tolerability of RGH-706 in people with Prader-Willi syndrome and will measure changes in hyperphagia, body weight, body mass, metabolism, and clinical global impression. (fpwr.org)
  • The results suggest that hyperphagia was the mechanism responsible for compensatory growth in Chinese shrimp. (bioone.org)
  • Importantly, EPM301 (20 and 40 mg/kg/d, i.p.) effectively reduced body weight and hyperphagia in a high-fat diet-fed Magel2 null mouse model for PWS. (nih.gov)
  • "This suggests that these elevations in peripheral endocannabinoid signalling are critical in driving hyperphagia associated with a western diet," ​ said study co-author Donovan Argueta, a bioengineering Ph.D. student. (foodnavigator.com)
  • Knockdown of AMPK reduced AMPK phosphorylation and food intake in non-transgenic flies , and further suppressed synphilin-1-induced AMPK phosphorylation , hyperphagia , fat storage and body weight gain in transgenic flies . (bvsalud.org)
  • Treatment with STO-609 also suppressed synphilin-1-induced AMPK phosphorylation , hyperphagia and body weight gain. (bvsalud.org)
  • Stress hyperphagia is often noticed in people operating under pressure. (medscape.com)
  • IQ testing was conducted in offspring, and parents completed questionnaires that tapped their child's compulsivity, hyperphagia, and other behavior problems. (nih.gov)
  • During hyperphagia, bears eat constantly and are always looking for a snack. (mycountry955.com)
  • The terms "hyperphagia" and "polyphagia" refer to someone who is focused only on eating, or who eats a large amount before feeling full. (medlineplus.gov)
  • Mallards may engage in hyperphagia in response to winter floods that temporarily make available more wetlands for foraging, heavily increasing their daily food intake to make use of the additional food. (wikipedia.org)
  • DESTINY PWS (C601) was an international, placebo-controlled, Phase 3 study of DCCR (diazoxide choline) extended-release tablet in participants with PWS, age 4 and older with hyperphagia. (endocrine-abstracts.org)
  • Conclusions: Subjects with AS have greater hyperphagia scores, higher leptin concentrations, and lower BDNF/leptin ratios than controls subjects of similar body size. (nih.gov)
  • During this time of low food availability, new cubs stay nourished thanks to their mother's rich milk, and adults rely on the fat reserves they built during hyperphagia the previous fall. (piquenewsmagazine.com)
  • The shrimp responded to a switch from starvation to ad libitum feeding by exhibiting hyperphagia and a growth spurt. (bioone.org)
  • In behavioral ecology, hyperphagia is a short-term increase in food intake and metabolization in response to changing environmental conditions. (wikipedia.org)