Prediabetic State
Glucose Tolerance Test
Mice, Inbred NOD
Diabetes Mellitus, Type 1
Rats, Zucker
Islets of Langerhans
Diabetes Mellitus, Type 2
Insulin
Rats, Inbred OLETF
Rats, Inbred BB
Appetite
Hypothyroidism
Thyroxine
Appetite Stimulants
Congenital Hypothyroidism
Early autoantibody responses in prediabetes are IgG1 dominated and suggest antigen-specific regulation. (1/617)
The islet autoimmunity of preclinical type 1 diabetes remains poorly characterized in humans. In this paper, the IgG subclass response to the islet autoantigens insulin, glutamic acid decarboxylase, and IA-2 was studied sequentially from birth to diabetes onset or current follow-up in 26 autoantibody positive offspring of parents with diabetes. Islet autoantibody appearance was characterized by an early IgG1 peak response to one or more Ags, most commonly to insulin, at a median age of 2.2 yr (interquartile range, 2-2.9 yr). In five offspring, an acute fulminant beta-cell destruction and diabetes onset occurred during this initial Ab response. In the remainder, early Ab levels declined markedly, and Ab peaks against other beta cell Ags arose sequentially over several years suggesting regulation and spreading of autoimmunity. Second peak Ab responses to the same Ag were observed in only two offspring, both developing diabetes at this time. Two others developed diabetes with declining Ab levels. Abs of IgG1 subclass dominated against each Ag, and other subclasses, were usually only detected during peak IgG1 responses. The IgG4 response to insulin was exceptional, being dominant over IgG1 in four offspring and in five others appeared and/or persisted after IgG1 levels declined. These Th2-associated IgG4 responses were not correlated with protection from diabetes. The presence of IgG1-restricted responses to DA2 were associated with diabetes development. These findings suggest that type 1 diabetes has an early acute destructive phase of beta cell autoimmunity, which may be regulated and which spreads chronically until diabetes onset. (+info)Exposure of human islets to cytokines can result in disproportionately elevated proinsulin release. (2/617)
Infiltration of immunocytes into pancreatic islets precedes loss of beta cells in type 1 diabetes. It is conceivable that local release of cytokines affects the function of beta cells before their apoptosis. This study examines whether the elevated proinsulin levels that have been described in prediabetes can result from exposure of beta cells to cytokines. Human beta-cell preparations were cultured for 48 or 72 hours with or without IL-1beta, TNF-alpha, or IFN-gamma, alone or in combination. None of these conditions were cytotoxic, nor did they reduce insulin biosynthetic activity. Single cytokines did not alter medium or cellular content in insulin or proinsulin. Cytokine combinations, in particular IL-1beta plus IFN-gamma, disproportionately elevated medium proinsulin levels. This effect expresses an altered functional state of the beta cells characterized by preserved proinsulin synthesis, a slower hormone conversion, and an increased ratio of cellular proinsulin over insulin content. The delay in proinsulin conversion can be attributed to lower expression of PC1 and PC2 convertases. It is concluded that disproportionately elevated proinsulin levels in pre-type 1 diabetic patients might result from exposure of their beta cells to cytokines released from infiltrating immunocytes. This hormonal alteration expresses an altered functional state of the beta cells that can occur independently of beta-cell death. (+info)IL-18 inhibits diabetes development in nonobese diabetic mice by counterregulation of Th1-dependent destructive insulitis. (3/617)
The development of type 1 diabetes in animal models is T cell and macrophage dependent. Islet inflammation begins as peripheral benign Th2 type insulitis and progresses to destructive Th1 type insulitis, which is driven by the innate immune system via secretion of IL-12 and IL-18. We now report that daily application of IL-18 to diabetes-prone female nonobese diabetic mice, starting at 10 wk of age, suppresses diabetes development (p < 0.001, 65% in sham-treated animals vs 33% in IL-18-treated animals by 140 days of age). In IL-18-treated animals, we detected significantly lower intraislet infiltration (p < 0.05) and concomitantly an impaired progression from Th2 insulitis to Th1-dependent insulitis, as evidenced from IFN-gamma and IL-10 mRNA levels in tissue. The deficient progression was probably due to lesser mRNA expression of the Th1 driving cytokines IL-12 and IL-18 by the innate immune system (p < 0.05). Furthermore, the mRNA expression of inducible NO synthase, a marker of destructive insulitis, was also not up-regulated in the IL-18-treated group. IL-18 did not exert its effect at the levels of islet cells. Cultivation of islets with IL-18 affected NO production or mitochondrial activity and did not protect from the toxicity mediated by IL-1beta, TNF-alpha, and IFN-gamma. In conclusion, we show for the first time that administration of IL-18, a mediator of the innate immune system, suppresses autoimmune diabetes in nonobese diabetic mice by targeting the Th1/Th2 balance of inflammatory immune reactivity in the pancreas. (+info)Isolation of self antigen-reactive cells from inflamed islets of nonobese diabetic mice using CD4high expression as a marker. (4/617)
The low precursor frequency of Ag-reactive CD4+ T cells has been a barrier to the study of CD4+ T cell responses to conventional Ags as well as CD4+ T cell responses to autoantigens recognized during the course of an autoimmune disease. We have recently reported that all "conventional Ag" reactive CD4+ T cells are contained within the subpopulation expressing high levels of the CD4 molecule, termed CD4high. We have identified a CD4high population in the islets of Langerhans of prediabetic nonobese diabetic (NOD) mice that is extremely potent in transferring disease. As few as 500 CD4high islet-infiltrating CD4+ T cells transferred insulin-dependent diabetes mellitus to CD8 reconstituted NOD-SCID mice within 30 days of transfer. In contrast, CD4high T cells isolated from either NOD spleen or salivary glands did not transfer insulin-dependent diabetes mellitus into similar CD8-reconstituted NOD-SCID recipients. These data indicate that the precursor frequency of NOD islet-reactive, pathogenic CD4+ T cells is much higher in the prediabetic NOD pancreas than in these other organs. The islet-infiltrating CD4high T cells displayed selected memory markers, by cell surface analysis, and displayed a Th 1 phenotype by RNase protection assay, but had a marked decrease in IL-4 mRNA determined by quantitative real time PCR when compared with the less pathogenic CD4normal islet-infiltrating T cells. Use of the CD4high marker to select Ag activated T cells represents a tool to isolate and study pathogenic CD4+ T cells from autoimmune lesions in which the Ag has not been previously defined. (+info)Circulating antibodies against an exocrine pancreatic enzyme in type 1 diabetes. (5/617)
In this article, we report the identification of a new autoantigen in type 1 diabetes originating from the exocrine pancreas. This antigen is a pancreatic enzyme termed bile salt-dependent lipase (BSDL). We show that antibodies present in the sera of newly diagnosed type 1 diabetic patients recognize BSDL and more specifically the COOH-terminal mucin-like region of the protein. Therefore, we engineered the COOH-terminal peptide of BSDL and demonstrated that autoreactivity was linked to specific glycosylation sites by at least two glycosyltransferases: the Core 2 beta(1-6)N-acetylglucosaminyltransferase and the alpha(1-3) fucosyltransferase FUT7. We next examined the prevalence of circulating anti-BSDL antibodies in type 1 diabetic patients and found 73.5% positivity (25 sera among 34 patients tested) at onset, whereas only 8.4% of normal individuals (7 of 83) were positive. Within a cohort of first-degree relatives of diabetic patients followed prospectively until development of diabetes, 6 of 19 (31.6%) were also positive. Interestingly, two prediabetic individuals were already positive for anti-BSDL antibodies (Abs), while islet cell cytoplasmic Abs and antibodies to GAD65, IA-2, and insulin were not detected. Anti-BSDL autoantibodies were weakly or not detected in patients suffering from pancreatitis or pancreatic adenocarcinoma or in patients with Graves' disease. Although autoreactivity to BSDL in prediabetic and newly diagnosed diabetic patients might reflect cross-reactivity, our results strongly suggest that in addition to pancreatic beta-cells, acinar cells may be also affected in type 1 diabetes. (+info)Alteration in aortic wall stiffness and accumulation of collagen during the prediabetic stage of type II diabetes mellitus in rats. (6/617)
Aortic damage during the prediabetic stage of diabetes mellitus (DM) was investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, as an animal model of type II DM. In 30 OLETF and 30 nonDM rats, an oral glucose tolerance test was performed at 10, 20 and 30 weeks of age. At 15 and 30 weeks, intravascular ultrasound images and aortic pressure were recorded and the stiffness parameter beta was calculated. The aortic walls were excised at 5, 15 and 30 weeks for histopathology and the measurement of hydroxyproline. At 10 weeks, blood glucose (mg/dl) and insulin concentrations (ng/ml) of the OLETF rats (2h; 168+/-30 and 0.82+/-0.15) were significantly high (nonDM: 118+/-15; p = 0.02 and 0.16+/-0.64; p = 0.003). At the prediabetic stage (15 weeks), beta in the OLETF rats (2.5+/-0.9) was larger than in nonDM rats (1.4+/-0.4; p = 0.0006), and the collagen (hydroxyproline) content/dry weight (mg/g) of the aortic wall was significantly higher in OLETF (33.5+/-3.1) than in nonDM rats (28.7+/-3.5; p<.05). Histopathological examination showed that from 15 weeks of age the medial wall thickness increased gradually. In the prediabetic stage, collagen accumulation may contribute to impairment of aortic wall stiffness in the OLETF rats, which would accelerate the aging process in the aortic wall. (+info)Alteration in left ventricular diastolic filling and accumulation of myocardial collagen at insulin-resistant prediabetic stage of a type II diabetic rat model. (7/617)
BACKGROUND: Considerable controversy exists regarding impairment of cardiac function in diabetes mellitus (DM). We investigated the serial changes in left ventricular (LV) histopathology and LV filling dynamics in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which have been established as an animal model of type II DM. METHODS AND RESULTS: In 54 OLETF and 54 non-DM rats, body weight, blood pressure, heart rate, and transmitral pulsed Doppler examinations were performed from 5 to 47 weeks of age. An oral glucose tolerance test was performed at 10, 20, and 30 weeks of age. The hearts were excised for histopathology, including immunohistochemistry and histomorphometry of collagen, and measurement of hydroxyproline at baseline and each stage of developing DM. In the prediabetic stage (15 weeks of age), in which fast blood glucose remained normal, OLETF rats manifested mild obesity, postprandial hyperglycemia, and hyperinsulinemia, and early diastolic transmitral inflow exhibited prolonged deceleration time (OLETF, 59+/-10 ms versus non-DM, 49+/-8 ms, P<0.01) and low peak velocity (OLETF, 73+/-11 cm/s versus non-DM, 88+/-11 cm/s, P<0.01). Histopathology revealed extracellular fibrosis and abundant transforming growth factor-beta(1) receptor II in LV myocytes of OLETF rats. At 15 weeks of age, the ratio of collagen area/visual field of LV wall in OLETF rats (8.3+/-1.3%) was larger than that in non-DM rats (4.9+/-1.8%, P<0.0001), and the collagen content/dry tissue weight ratio of heart was significantly higher in OLETF (2. 0+/-0.5 mg/g) than non-DM (1.3+/-0.2 mg/g, P<0.01) rats. CONCLUSIONS: A metabolic abnormality present in the prestage of type II DM may produce LV fibrosis and alteration in cardiac function. (+info)B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes. (8/617)
CD28/B7 costimulation has been implicated in the induction and progression of autoimmune diseases. Experimentally induced models of autoimmunity have been shown to be prevented or reduced in intensity in mice rendered deficient for CD28 costimulation. In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. These cells are absent from both CD28KO and B7-1/B7-2KO mice, and the transfer of this regulatory T cell subset from control NOD animals into CD28-deficient animals can delay/prevent diabetes. The results suggest that the CD28/ B7 costimulatory pathway is essential for the development and homeostasis of regulatory T cells that control spontaneous autoimmune diseases. (+info)A prediabetic state, also known as impaired glucose tolerance or prediabetes, is a metabolic condition where blood sugar levels are higher than normal but not high enough to meet the diagnostic criteria for diabetes. It is often characterized by insulin resistance and beta-cell dysfunction, which can lead to an increased risk of developing type 2 diabetes, cardiovascular disease, and other complications if left untreated.
In the prediabetic state, fasting plasma glucose levels are between 100 and 125 mg/dL (5.6-6.9 mmol/L), or hemoglobin A1c (HbA1c) levels are between 5.7% and 6.4%. Lifestyle modifications, such as regular exercise, healthy eating habits, and weight loss, can help prevent or delay the progression of prediabetes to diabetes.
A Glucose Tolerance Test (GTT) is a medical test used to diagnose prediabetes, type 2 diabetes, and gestational diabetes. It measures how well your body is able to process glucose, which is a type of sugar.
During the test, you will be asked to fast (not eat or drink anything except water) for at least eight hours before the test. Then, a healthcare professional will take a blood sample to measure your fasting blood sugar level. After that, you will be given a sugary drink containing a specific amount of glucose. Your blood sugar levels will be measured again after two hours and sometimes also after one hour.
The results of the test will indicate how well your body is able to process the glucose and whether you have normal, impaired, or diabetic glucose tolerance. If your blood sugar levels are higher than normal but not high enough to be diagnosed with diabetes, you may have prediabetes, which means that you are at increased risk of developing type 2 diabetes in the future.
It is important to note that a Glucose Tolerance Test should be performed under the supervision of a healthcare professional, as high blood sugar levels can be dangerous if not properly managed.
Inbred NOD (Nonobese Diabetic) mice are a strain of laboratory mice that are genetically predisposed to develop autoimmune diabetes. This strain was originally developed in Japan and has been widely used as an animal model for studying type 1 diabetes and its complications.
NOD mice typically develop diabetes spontaneously at around 12-14 weeks of age, although the onset and severity of the disease can vary between individual mice. The disease is caused by a breakdown in immune tolerance, leading to an autoimmune attack on the insulin-producing beta cells of the pancreas.
Inbred NOD mice are highly valuable for research purposes because they exhibit many of the same genetic and immunological features as human patients with type 1 diabetes. By studying these mice, researchers can gain insights into the underlying mechanisms of the disease and develop new treatments and therapies.
Diabetes Mellitus, Type 1 is a chronic autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas, leading to an absolute deficiency of insulin. This results in an inability to regulate blood glucose levels, causing hyperglycemia (high blood sugar). Type 1 diabetes typically presents in childhood or early adulthood, although it can develop at any age. It is usually managed with regular insulin injections or the use of an insulin pump, along with monitoring of blood glucose levels and adjustments to diet and physical activity. Uncontrolled type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, blindness, and cardiovascular disease.
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.
The Islets of Langerhans are clusters of specialized cells within the pancreas, an organ located behind the stomach. These islets are named after Paul Langerhans, who first identified them in 1869. They constitute around 1-2% of the total mass of the pancreas and are distributed throughout its substance.
The Islets of Langerhans contain several types of cells, including:
1. Alpha (α) cells: These produce and release glucagon, a hormone that helps to regulate blood sugar levels by promoting the conversion of glycogen to glucose in the liver when blood sugar levels are low.
2. Beta (β) cells: These produce and release insulin, a hormone that promotes the uptake and utilization of glucose by cells throughout the body, thereby lowering blood sugar levels.
3. Delta (δ) cells: These produce and release somatostatin, a hormone that inhibits the release of both insulin and glucagon and helps regulate their secretion in response to changing blood sugar levels.
4. PP cells (gamma or γ cells): These produce and release pancreatic polypeptide, which plays a role in regulating digestive enzyme secretion and gastrointestinal motility.
Dysfunction of the Islets of Langerhans can lead to various endocrine disorders, such as diabetes mellitus, where insulin-producing beta cells are damaged or destroyed, leading to impaired blood sugar regulation.
Diabetes Mellitus, Type 2 is a metabolic disorder characterized by high blood glucose (or sugar) levels resulting from the body's inability to produce sufficient amounts of insulin or effectively use the insulin it produces. This form of diabetes usually develops gradually over several years and is often associated with older age, obesity, physical inactivity, family history of diabetes, and certain ethnicities.
In Type 2 diabetes, the body's cells become resistant to insulin, meaning they don't respond properly to the hormone. As a result, the pancreas produces more insulin to help glucose enter the cells. Over time, the pancreas can't keep up with the increased demand, leading to high blood glucose levels and diabetes.
Type 2 diabetes is managed through lifestyle modifications such as weight loss, regular exercise, and a healthy diet. Medications, including insulin therapy, may also be necessary to control blood glucose levels and prevent long-term complications associated with the disease, such as heart disease, nerve damage, kidney damage, and vision loss.
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.
Blood glucose, also known as blood sugar, is the concentration of glucose in the blood. Glucose is a simple sugar that serves as the main source of energy for the body's cells. It is carried to each cell through the bloodstream and is absorbed into the cells with the help of insulin, a hormone produced by the pancreas.
The normal range for blood glucose levels in humans is typically between 70 and 130 milligrams per deciliter (mg/dL) when fasting, and less than 180 mg/dL after meals. Levels that are consistently higher than this may indicate diabetes or other metabolic disorders.
Blood glucose levels can be measured through a variety of methods, including fingerstick blood tests, continuous glucose monitoring systems, and laboratory tests. Regular monitoring of blood glucose levels is important for people with diabetes to help manage their condition and prevent complications.
"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.
I'm sorry for any confusion, but "Rats, Inbred BB" is not a widely recognized medical term or abbreviation in human or veterinary medicine. The term "inbred" is used in genetics to describe an organism that has resulted from many generations of mating between closely related individuals, which can lead to a higher incidence of homozygosity (the same allele inherited from both parents) and expression of recessive traits.
The "BB" strain could refer to a specific inbred rat strain, but without more context, it's difficult to provide a precise definition. The BB Wistar rat strain is sometimes used in research, and it has been used as a model for studying various medical conditions such as diabetes and hypertension.
If you are looking for information about a specific scientific study or medical condition related to an "Inbred BB" rat strain, I would be happy to help you if you could provide more context or details.
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.
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.
Hypothyroidism is a medical condition where the thyroid gland, which is a small butterfly-shaped gland located in the front of your neck, does not produce enough thyroid hormones. This results in a slowing down of the body's metabolic processes, leading to various symptoms such as fatigue, weight gain, constipation, cold intolerance, dry skin, hair loss, muscle weakness, and depression.
The two main thyroid hormones produced by the thyroid gland are triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating various bodily functions, including heart rate, body temperature, and energy levels. In hypothyroidism, the production of these hormones is insufficient, leading to a range of symptoms that can affect multiple organ systems.
Hypothyroidism can be caused by several factors, including autoimmune disorders (such as Hashimoto's thyroiditis), surgical removal of the thyroid gland, radiation therapy for neck cancer, certain medications, and congenital defects. Hypothyroidism is typically diagnosed through blood tests that measure levels of TSH (thyroid-stimulating hormone), T3, and T4. Treatment usually involves taking synthetic thyroid hormones to replace the missing hormones and alleviate symptoms.
Thyroxine (T4) is a type of hormone produced and released by the thyroid gland, a small butterfly-shaped endocrine gland located in the front of your neck. It is one of two major hormones produced by the thyroid gland, with the other being triiodothyronine (T3).
Thyroxine plays a crucial role in regulating various metabolic processes in the body, including growth, development, and energy expenditure. Specifically, T4 helps to control the rate at which your body burns calories for energy, regulates protein, fat, and carbohydrate metabolism, and influences the body's sensitivity to other hormones.
T4 is produced by combining iodine and tyrosine, an amino acid found in many foods. Once produced, T4 circulates in the bloodstream and gets converted into its active form, T3, in various tissues throughout the body. Thyroxine has a longer half-life than T3, which means it remains active in the body for a more extended period.
Abnormal levels of thyroxine can lead to various medical conditions, such as hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). These conditions can cause a range of symptoms, including weight gain or loss, fatigue, mood changes, and changes in heart rate and blood pressure.
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 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.
Congenital hypothyroidism is a medical condition characterized by the partial or complete absence of thyroid hormone production in the baby's body at birth. The thyroid gland, which is located in the front of the neck, produces hormones that are essential for normal growth and development of the brain and body.
Congenital hypothyroidism can occur due to various reasons such as the absence or abnormal development of the thyroid gland, or a defect in the production or regulation of thyroid hormones. In some cases, it may be caused by genetic mutations that affect the development or function of the thyroid gland.
If left untreated, congenital hypothyroidism can lead to mental and physical retardation, growth problems, and other health issues. Therefore, it is important to diagnose and treat this condition as early as possible, usually within the first few weeks of life. Treatment typically involves replacing the missing thyroid hormones with synthetic medications, which are safe and effective when administered under a doctor's supervision.
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Obese3
- Research design and methods The aim of this study was to investigate the effects of compositions derived from three strains of F. prausnitzii (coined FPZ) on glucose metabolism in diet-induced obese male C57BL/6J prediabetic and type 2 diabetic mice. (bmj.com)
- I highly recommend this review to anyone with a background in the biological sciences who wants to understand how leptin works in both the lean and obese state. (blogspot.com)
- Obese-prediabetic mice continued to exhibit impaired Ach-dependent vasodilation but PIV appeared normalized. (iah2010.org)
Glucose Tole1
- The pre-diabetic state, defined by an oral glucose tolerance test (OGTT), includes impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or their combination ( 2 ). (diabetesjournals.org)
Diabetic patients3
- We've shown in multiple studies that the exact same pathophysiologic disturbances are present in prediabetic and diabetic patients. (medscape.com)
- However, dysregulation of the HPA axis in T2DM has been shown to worsen further the hyperglycaemic state causing hyperlipidemia and dyslipidemia as well as increase the risk of depression in diabetic patients (8, 13-16). (researchsquare.com)
- Medical nutrition therapy is extremely important for diabetic patients and prediabetic patients so that adequate glycemic control can be achieved. (medscape.com)
Obesity1
- Numerous studies have correlated the reduction of F. prausnitzii abundance with many disease states, including irritable bowel syndrome, Crohn's disease, obesity, asthma, major depressive disorder, and metabolic diseases in humans. (bmj.com)
Hyperglycemia1
- When insulin is unable to induce glucose uptake, pancreatic beta-cells increase insulin production and the hyperinsulinemic state prevents hyperglycemia. (isciii.es)
Intervention1
- As such, evidence to date suggests that we are able to identify individuals in "prediabetic states" and that we can delay the progression to overt diabetes, at least as documented with intervention strategies tested in well-designed clinical trials. (diabetesjournals.org)
Tolerance2
- People with impaired glucose tolerance, a "prediabetic state" numbered 308 million in 2007 and will increase to 418 million by 2025 [5]. (ispub.com)
- Results Both trials in prediabetic and diabetic mice revealed that peroral administration of live FPZ or extracts from FPZ lowered fasting blood glucose levels and improved glucose tolerance compared with control mice. (bmj.com)
Diabetes11
- Bustan RS, Wasim D, Yderstræde KB, Bygum A. Specific skin signs as a cutaneous marker of diabetes mellitus and the prediabetic state - a systematic review. (medscape.com)
- Pre-diabetes is defined as an intermediary state of hyperglycaemia that occurs between normoglycaemia and type 2 diabetes mellitus (T2DM) with blood glucose concentrations above normal but below the threshold for diagnosis of diabetes (1, 2). (researchsquare.com)
- The working hypothesis is that alterations in pyruvate metabolism will contribute to balancing redox state and alleviating oxidative stress leading to improvement of cardiac function during diabetes. (unl.edu)
- The abundance of commensal bacteria such as Faecalibacterium prausnitzii shows negative correlations with many disease states but lacks experimental data showing that administration of these live or killed beneficial bacteria will lead to health benefits, such as treatment of pre-diabetes and type 2 diabetes (T2D). (bmj.com)
- In the prediabetic state, type 2 diabetes involves two defects, peripheral insulin resistance and hyperinsulinemia, which is followed by the failure of insulin secretion to compensate for the insulin resistance. (medscimonit.com)
- Type 2 diabetes is preceded by a long pre-diabetic state, characterized by mild elevation of fasting and/or postprandial glucose levels. (diabetesjournals.org)
- Diabetes is a terrible disease that is one of the leading causes of death and disability in the United States and is the leading cause of amputation. (thelegacycenter.net)
- Oklahoma has one of the highest rates of diabetes in the nation - some 278,000 people have been diagnosed, another 113,400 are undiagnosed and yet another 678,000 are considered pre-diabetic, according to statistics from the Oklahoma State Department of Health. (journalrecord.com)
- Staff members of the Harold Hamm Oklahoma Diabetes Center in Oklahoma City are putting their hope, and their hard work, into a paradox - that in a state where diabetes is most prevalent, the biggest solutions to the disease may be found. (journalrecord.com)
- As we will see, diabetes and the peri-diabetic state is hell on the kidneys. (robbwolf.com)
- An estimated 1 in 3 children born in the United States in 2000 will develop type 2 diabetes at some point in their lifetime (4). (cdc.gov)
Rats1
- Sprague Dawley Rats were randomly divided into non-prediabetic group (NPD) and pre-diabetic group (PD) (n=6, per group) over a 20-week induction period and a further 12-week experimental period to get 32 weeks. (researchsquare.com)
Diabetics1
- There were 298 persons who were initially identified as diabetics but who were either borderline or prediabetic, who were only diabetic during pregnancy and never confirmed after pregnancy (some were still pregnant), or who denied that they were ever or currently diabetic. (cdc.gov)
Mice3
- Removing the LepR receptors and impairing leptin transport to the brain therefore led the mice to initially develop a pre-diabetic state. (medicalxpress.com)
- Conclusions The trial results have shown that treatment with different formulations of FPZ result in lower blood glucose levels, lower percent HbA1c, and improved glucose response in mice compared with control prediabetic/diabetic mice. (bmj.com)
- This study demonstrates that administering strains of the commensal F. prausnitzii or its extracts reduces fasting blood glucose, improves glucose response, and lowers percent HbA1c in prediabetic and diabetic mice without triggering hypoglycemia in mice with normal blood glucose levels. (bmj.com)
Diet1
- Stated another way, the increased palatability of the diet initiates a vicious cycle in which hedonics cause more food to be eaten than is necessary to meet energy needs, and the increased calories in turn initiate events that lead to insulin/leptin resistance and a consequent tendency to eat even more food (Figure 4). (blogspot.com)
Population2
- When this statistic is applied to the entire U.S. population in 2010, it would suggest that prediabetic states exist in an estimated 79 million Americans aged 20 years or older ( 1 ). (diabetesjournals.org)
- The NHIS is a personal interview household survey which uses a nationwide sample of the civilian, noninstitutionalized population of the United States. (cdc.gov)
Subjects1
- A pre-diabetic state and osteoporosis was induced in rodent subjects for both of the studies. (vitanetonline.com)
Involves1
- The agreement calls for the tribe to adopt and enforce the state of Oklahoma's environmental standards and substantive rules on Citizen Potawatomi trust lands in a cooperative and transparent manner that involves state agencies and the tribe's department of environmental protection. (journalrecord.com)
Patients2
- She said patients with prediabetic symptoms presented the most common ailment the group saw. (gram.edu)
- Fast Five Quiz: Nutritional Concerns From the management of diabetic and prediabetic patients to concerns about patients in a rehabilitation setting, test your knowledge of key aspects of nutritional management with this quick quiz. (medscape.com)
Occurs1
- Other situation where this problem occurs is in pre-diabetic state. (ndtv.com)
Million1
- 90 million peo- agents likely determine more cancers, immune-mediated ple in the United States) and are a rapidly growing burden syndromes, neurodevelopmental disorders, and other in developing economies (http://www.cdc.gov/nccdphp/ chronic conditions than currently appreciated. (cdc.gov)
Workplace1
- In a sample that is predominantly sedentary, at risk for cardiovascular disease, and prediabetic, there are no significant associations between workplace sedentary behavior and physiological markers. (cdc.gov)
Clinic1
- State mandated health screening for vision, hearing and Acanthosis Nigricans ( non-invasive prediabetic screening) have begun in the TES Clinic this month. (smore.com)
Kidneys1
- The hyperinsulinemic state induces several abnormalities in the liver, endothelium, and kidneys, and is the main feature in the metabolic syndrome. (isciii.es)
People2
- In the United States, about 659,000 people die from CVDs each year, which constitutes one in every four deaths. (unl.edu)
- Did you know that 1 in 4 people in the United States are pre-diabetic? (thelegacycenter.net)
Control1
- Beyond performance and alertness, if you measure blood glucose and testosterone levels before and after five nights of five hours sleep in an otherwise healthy young man, glucose control diminishes to a level comparable to a prediabetic state and testosterone levels fall as though he has aged a decade. (sydneyoperahouse.com)
Services1
- CVDs costs the United States about $363 billion each year, which includes the cost of health care services, medicines, and lost productivity due to death. (unl.edu)
Students3
- All students in Kinder, First and Third grade, as well as any new students to Tomball ISD, will be screened per state guidelines. (smore.com)
- Pictured are the eight Grambling State University students who served a two-week internship in Peru earlier this summer as part of a medical outreach program. (gram.edu)
- Eight Grambling State University (GSU) students spent a couple of weeks in Cusco, Peru, this summer for an internship program serving more than 150 residents of that nation with a medical outreach program. (gram.edu)
Year2
- Last year, Grambling State senior biology major Andreanna Wright from Madison, Wisconsin, was assigned the role of Team Leader for the VAW Global Health Alliances Medical Chapter at GSU and through that organization set up the GSU internship program. (gram.edu)
- A 22-Year-Old Traveler With Altered Mental Status A 22-year-old man with no significant medical history is transferred from the airport in a semiconscious state after returning from a 3-week vacation. (medscape.com)
Figure1
- 1989). The frequency of these sites within the United States can be seen in Figure 5-l. (cdc.gov)