Severe HYPOGLYCEMIA induced by a large dose of exogenous INSULIN resulting in a COMA or profound state of unconsciousness from which the individual cannot be aroused.
A profound state of unconsciousness associated with depressed cerebral activity from which the individual cannot be aroused. Coma generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the brain stem RETICULAR FORMATION.
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).
A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE.
A scale that assesses the response to stimuli in patients with craniocerebral injuries. The parameters are eye opening, motor response, and verbal response.
A state of unconsciousness as a complication of diabetes mellitus. It occurs in cases of extreme HYPERGLYCEMIA or extreme HYPOGLYCEMIA as a complication of INSULIN therapy.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
A structurally-related group of signaling proteins that are phosphorylated by the INSULIN RECEPTOR PROTEIN-TYROSINE KINASE. The proteins share in common an N-terminal PHOSPHOLIPID-binding domain, a phosphotyrosine-binding domain that interacts with the phosphorylated INSULIN RECEPTOR, and a C-terminal TYROSINE-rich domain. Upon tyrosine phosphorylation insulin receptor substrate proteins interact with specific SH2 DOMAIN-containing proteins that are involved in insulin receptor signaling.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.

Clinical characteristics of type 1 diabetic patients with and without severe hypoglycemia. (1/17)

OBJECTIVE: To investigate the frequency of severe hypoglycemia (SH) and hypoglycemic coma and to identify clinical and behavioral risk indicators in a nonselected population of type 1 diabetic patients. RESEARCH DESIGN AND METHODS: This study involved a retrospective clinical survey of 195 consecutive patients using a questionnaire addressing the frequency of SH (i.e., help from others required) and hypoglycemic coma during the previous year, general characteristics, behavior, hypoglycemia awareness, and the Hypoglycemia Fear Survey Data regarding diabetes, treatment, long-term complications, comorbidity, and comedication were obtained from the patients' medical records. RESULTS: A total of 82% of subjects were receiving intensive insulin treatment, and mean +/- SD HbA(1c) was 7.8 +/- 1.2%. Mean duration of diabetes was 20 +/- 12 years. The occurrence of SH (including hypoglycemic coma) was 150 episodes/100 patient-years and affected 40.5% of the population. Hypoglycemic coma occurred in 19% of subjects (40 episodes/100 patient-years). SH without coma was independently related to nephropathy (odds ratio [OR] 4.8 [95% CI 1.5-15.1]), a threshold for hypoglycemic symptoms of <3 mmol/l (4.8 [1.8-12.0]), and a daily insulin dose 0.1 U/kg higher (1.3 [1.0-1.6]) (all ORs were adjusted for diabetes duration and use of comedication). Hypoglycemic coma was independently related to neuropathy (3.9 [1.5-10.4]), (nonselective) beta-blocking agents (14.9 [2.1-107.4]), and alcohol use (3.5 [1.3-9.1]) (all ORs were adjusted for diabetes duration). CONCLUSIONS: SH and hypoglycemic coma are common in a nonselected population with type 1 diabetes. The presence of long-term complications, a threshold for symptoms of <3 mmo/l, alcohol use, and (nonselective) beta-blockers were associated with SH during the previous year. If prospectively confirmed, these results may have consequences for clinical practice.  (+info)

Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma. (2/17)

In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma. Two hours after the ischemic insults, the level of brain-derived neurotrophic factor (BDNF) mRNA was markedly increased in the granule cells of the dentate gyrus, and at 24 h it was still significantly elevated. NGF mRNA showed a pronounced increase 4 h after 2 min of ischemia but had returned to a control level at 24 h. Both 2 and 10 min of ischemia caused a clear reduction of the level of mRNA for neurotrophin 3 (NT-3) in the dentate granule cells and in regions CA2 and medial CA1 of the hippocampus 2 and 4 h after the insults. The increase of BDNF mRNA could be partially blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX but was not influenced by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Both NBQX and MK-801 attenuated the decrease of NT-3 mRNA after ischemia. One and 30 min of hypoglycemic coma also induced marked increases in BDNF and NGF mRNA in dentate granule cells with maximal levels at 2 h. If the changes of mRNA expression lead to alterations in the relative availability of neurotrophic factors, this could influence functional outcome and neuronal necrosis following ischemic and hypoglycemic insults.  (+info)

[Treatment of type 1 diabetes mellitus revealed below 7 years of age in the Diabetes Center of Silesia, Poland]. (3/17)

INTRODUCTION: Frequency of type 1 diabetes mellitus diagnosis in young children increases. Within this group, such factors as limited cooperation, little acceptance of multiple injections and other typical patterns of behavior can strongly influence the insulin management outcome. AIM OF THE STUDY: The objective of the study was to provide information regarding metabolic control in young diabetes patients. MATERIAL AND METHODS: Charts of 58 children with T1DM, all subjects under control of our Department, that were aged at onset (1998-2003) below 7 years (mean 4.05+/-1.6) were studied retrospectively. HbA1c, total, bolus and basal daily insulin requirement (DIR), weight, height, severe hypoglycaemia and diabetic ketoacidosis (DKA) were analyzed till April 2006 in 2-year intervals. Insulin therapy model was also taken into consideration. RESULTS: Mean HbA1c was 7.2+/-1.2% for all children for the whole studied period and did not alter significantly between analyzed intervals. Most common treatment model at diabetes onset was the therapy with premixed insulin (Mix) (67%) and after 4 and 6 years - continuous subcutaneous insulin infusion (CSII) (50% and 75% respectively). A tendency for a better metabolic control was observed at multiple daily injections and CSII than at Mix. Change of the weight or height percentile channel was not revealed. Bolus and basal DIR increased in the first observation interval. Afterwards they stabilized respectively at 0.35-0.42 U/kg/24 h and 0.35-0.39 U/kg/24 h. Severe hypoglycaemia occurred 6.72/100 patient-years. CONCLUSION: Insulin therapy aimed at maintaining long-term good metabolic control is possible to achieve and is safe in young diabetic children.  (+info)

Utility values for symptomatic non-severe hypoglycaemia elicited from persons with and without diabetes in Canada and the United Kingdom. (4/17)

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Hypoglycemia in type 1 diabetic pregnancy: role of preconception insulin aspart treatment in a randomized study. (5/17)

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Severe hypoglycaemia in drug-treated diabetic patients needs attention: a population-based study. (6/17)

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Extracellular pH in the rat brain during hypoglycemic coma and recovery. (7/17)

It has previously been shown that hypoglycemic coma is accompanied by marked energy failure and by loss of cellular ionic homeostasis. The general proposal is that shortage of carbohydrate substrate prevents lactic acid formation and thereby acidosis during hypoglycemic coma. The objective of the present study was to explore whether rapid downhill ion fluxes, known to occur during coma, are accompanied by changes in extra- and/or intracellular pH (pHe and/or pHi), and how these relate to the de- and repolarization of cellular membranes. Cortical pHe was recorded by microelectrodes in insulin-injected rats subjected to 30 min of hypoglycemic coma, with cellular membrane depolarization. Some rats were allowed up to 180 min of recovery after glucose infusion and membrane repolarization. Arterial blood gases and physiological parameters were monitored to maintain normotension, normoxia, normocapnia, and normal plasma pH. Following depolarization during hypoglycemia, a prompt, rapidly reversible alkaline pHe shift of about 0.1 units was observed in 37/43 rats. Immediately thereafter, all rats showed an acid pH shift of about 0.2 units. This shift developed during the first minute, and pHe remained at that level until repolarization was induced. Following repolarization, there was an additional, rapid, further lowering of pHe by about 0.05 units, followed by a more prolonged decrease in pHe that was maximal at 90 min of recovery (delta pHe of approximately -0.4 units). The pHe then slowly normalized but was still decreased (-0.18 pH units) after 180 min when the experiment was terminated. The calculated pHi showed no major alterations during hypoglycemic coma or after membrane repolarization following glucose administration.(ABSTRACT TRUNCATED AT 250 WORDS)  (+info)

Cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma. (8/17)

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.  (+info)

An Insulin Coma is not a formal medical term, but it has been used in the past to describe a deliberate medical procedure known as Insulin Shock Therapy. This was a treatment for mental illness that involved administering large doses of insulin to induce hypoglycemia (low blood sugar), which could lead to a coma.

The idea behind this therapy, which was popular in the mid-20th century, was that the induced coma and subsequent recovery could have therapeutic effects on the brain and help alleviate symptoms of mental illnesses like schizophrenia. However, this treatment fell out of favor due to its significant risks and the development of more effective and safer treatments.

It's important to note that in current medical practice, inducing a coma with insulin is not a standard or recommended procedure due to the potential for severe harm, including brain damage and death.

A coma is a deep state of unconsciousness in which an individual cannot be awakened, cannot respond to stimuli, and does not exhibit any sleep-wake cycles. It is typically caused by severe brain injury, illness, or toxic exposure that impairs the function of the brainstem and cerebral cortex.

In a coma, the person may appear to be asleep, but they are not aware of their surroundings or able to communicate or respond to stimuli. Comas can last for varying lengths of time, from days to weeks or even months, and some people may emerge from a coma with varying degrees of brain function and disability.

Medical professionals use various diagnostic tools and assessments to evaluate the level of consciousness and brain function in individuals who are in a coma, including the Glasgow Coma Scale (GCS), which measures eye opening, verbal response, and motor response. Treatment for coma typically involves supportive care to maintain vital functions, manage any underlying medical conditions, and prevent further complications.

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.

An insulin receptor is a transmembrane protein found on the surface of cells, primarily in the liver, muscle, and adipose tissue. It plays a crucial role in regulating glucose metabolism in the body. When insulin binds to its receptor, it triggers a series of intracellular signaling events that promote the uptake and utilization of glucose by cells, as well as the storage of excess glucose as glycogen or fat.

Insulin receptors are composed of two extracellular alpha subunits and two transmembrane beta subunits, which are linked together by disulfide bonds. The binding of insulin to the alpha subunits activates the tyrosine kinase activity of the beta subunits, leading to the phosphorylation of intracellular proteins and the initiation of downstream signaling pathways.

Abnormalities in insulin receptor function or number can contribute to the development of insulin resistance and type 2 diabetes.

The Glasgow Coma Scale (GCS) is a standardized tool used by healthcare professionals to assess the level of consciousness and neurological response in a person who has suffered a brain injury or illness. It evaluates three aspects of a patient's responsiveness: eye opening, verbal response, and motor response. The scores from these three categories are then added together to provide an overall GCS score, which can range from 3 (indicating deep unconsciousness) to 15 (indicating a normal level of consciousness). This scale helps medical professionals to quickly and consistently communicate the severity of a patient's condition and monitor their progress over time.

A diabetic coma is a serious and life-threatening condition that occurs when an individual with diabetes experiences severely high or low blood sugar levels, leading to unconsciousness. It is a medical emergency that requires immediate attention.

In the case of hyperglycemia (high blood sugar), the body produces excess amounts of urine to try to eliminate the glucose, leading to dehydration and a lack of essential nutrients in the body. This can result in a buildup of toxic byproducts called ketones, which can cause a condition known as diabetic ketoacidosis (DKA). DKA can lead to a diabetic coma if left untreated.

On the other hand, hypoglycemia (low blood sugar) can also cause a diabetic coma. This occurs when the brain is not receiving enough glucose to function properly, leading to confusion, seizures, and eventually unconsciousness.

If you suspect someone is experiencing a diabetic coma, it is important to seek emergency medical attention immediately. While waiting for help to arrive, try to administer glucose or sugar to the individual if they are conscious and able to swallow. If they are unconscious, do not give them anything to eat or drink, as this could cause choking or further complications.

Insulin resistance is a condition in which the body's cells become less responsive to insulin, a hormone produced by the pancreas that regulates blood sugar levels. In response to this decreased sensitivity, the pancreas produces more insulin to help glucose enter the cells. However, over time, the pancreas may not be able to keep up with the increased demand for insulin, leading to high levels of glucose in the blood and potentially resulting in type 2 diabetes, prediabetes, or other health issues such as metabolic syndrome, cardiovascular disease, and non-alcoholic fatty liver disease. Insulin resistance is often associated with obesity, physical inactivity, and genetic factors.

Insulin Receptor Substrate (IRS) proteins are a family of cytoplasmic signaling proteins that play a crucial role in the insulin signaling pathway. There are four main isoforms in humans, namely IRS-1, IRS-2, IRS-3, and IRS-4, which contain several conserved domains for interacting with various signaling molecules.

When insulin binds to its receptor, the intracellular tyrosine kinase domain of the receptor becomes activated and phosphorylates specific tyrosine residues on IRS proteins. This leads to the recruitment and activation of downstream effectors, such as PI3K and Grb2/SOS, which ultimately result in metabolic responses (e.g., glucose uptake, glycogen synthesis) and mitogenic responses (e.g., cell proliferation, differentiation).

Dysregulation of the IRS-mediated insulin signaling pathway has been implicated in several pathological conditions, including insulin resistance, type 2 diabetes, and certain types of cancer.

Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.

In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.

Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.

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