Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The allocation of hypoglycaemic symptoms to autonomic or neuroglycopenic groups tends to occur on an a priori basis. In view of the practical need for clear symptom markers of hypoglycaemia more scientific approaches must be pursued. Substantial evidence is presented from two large scale studies we performed which support a three factor model of hypoglycaemic symptomatology, based on the statistical associations discovered among symptoms reported by diabetic patients. Study 1 involved 295 insulin-treated out-patients and found that 11 key hypoglycaemic symptoms segregated into three clear factors: autonomic (sweating, palpitation, shaking and hunger) neuroglycopenic (confusion, drowsiness, odd behaviour, speech difficulty and incoordination), and malaise (nausea and headache). The three factors were validated on a separate group of 303 insulin-treated diabetic out-patients. Confirmatory factor analyses showed that the three factor model was the optimal model for explaining symptom covariance in each group. A multi-sample confirmatory factor analysis tested the rigorous assumptions that the relative loadings of symptoms on factors across groups were equal, and that the residual variance for each symptom was identical across groups. These assumptions were successful, indicating that the three factor model was replicated in detail across these two large samples. It is suggested that the results indicate valid groupings of symptoms that may be used in future research and in clinical practice.
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PMID:Partitioning the symptoms of hypoglycaemia using multi-sample confirmatory factor analysis. 840 46

Biochemical hypoglycemia has attracted attention because it triggers accidents through errors in judgment by impairing cognitive function. Its prevalence and associated risk factors have remained unexplored in the area of occupational health. The present study was designed to investigate its epidemiological aspects in male volunteers. The study population of 76 male volunteers, 63 of whom were firefighters and 13 had other jobs, filled out questionnaires by interview covering 37 factors concerning age, physical parameters, past and current health problems, habits (smoking, drinking, and exercise), food preferences and life style. The participants were asked to measure their blood glucose levels 9 times over a representative workday and holiday and record any symptoms of hypoglycemia at the time of measurement. The body fat ratio of each participant was measured by the bioelectrical impedance analysis method. 22.4% of the participants (17/76) experienced biochemical hypoglycemia (less than 60 mg/dl) at the time of blood glucose monitoring. Those who experienced biochemical hypoglycemia had significantly lower peak, average and nadir blood glucose levels (p < 0.05; 115.1 +/- 18.7 mg/dl, 82.2 +/- 7.0 mg/dl, 52.2 +/- 5.6 mg/dl, respectively) than those who did not (129.9 +/- 26.7 mg/dl, 97.0 +/- 9.9 mg/dl, 75.9 +/- 9.7 mg/dl, respectively). No symptom other than sudden hunger (p < 0.05) was correlated with biochemical hypoglycemia. Lower lean body mass index (lean body mass/height2) was the only statistically significant contributory risk factor (p < 0.05, Odds ratio: 2.91, 95% confidence interval 1.29-6.65) by multiple logistic analysis. Mean blood glucose levels had a positive correlation with lean body mass index (P < 0.0001, r2 = 0.372). The present results suggest that biochemical hypoglycemia is a potential risk problem in occupational settings. Low L.B.M.I. males should be educated about the possibility of biochemical hypoglycemia whoever have experienced a feeling of sudden hunger. Such precautions should be highly recommended to workers under dangerous and/or tense conditions in order to prevent error accidents in occupational settings.
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PMID:An endemic condition of biochemical hypoglycemia among male volunteers. 890 43

The effects of four equienergetic breakfasts with varying fiber and macronutrient contents on hunger and satiety ratings, on subsequent lunch intake, and on postprandial carbohydrate and fat metabolism were investigated in normal weight male subjects in two experiments, in which lunch was offered at a predetermined time (Experiment 1) or in which the subjects were free to choose when to eat lunch (Experiment 2). Consumption of either a commercially available high fiber cereal (HFC, 10% fiber), a medium fiber cereal (MFC, 7% fiber), a low fiber cereal (LFC, 3% fiber), or a standard continental breakfast (0% fiber) on nonconsecutive days did not differentially affect hunger and satiety ratings, the size or microstructure of the subsequent lunch, and the breakfast to lunch intermeal interval (in Experiment 2). Plasma concentrations of glucose, lactate, and insulin increased more after the LFC breakfast than after the other breakfast varieties. A reactive postprandial hypoglycaemia occurred after the LFC breakfast, shortly before lunch. The plasma concentrations of fat metabolites (triglycerides, free fatty acids, beta-hydroxybutyrate) and of glucagon were not differentially affected by the breakfast varieties. The results are consistent with the assumption that energy content of a meal is the major determinant of subsequent energy intake in man and the fiber content and macronutrient composition have only a modulating effect.
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PMID:Breakfasts with different fiber and macronutrient contents do not differentially affect timing, size or microstructure of the subsequent lunch. 900 Mar 33

Symptomatic episodes of documented hypoglycaemia were characterized with the aid of a 3-month diary in a single-centre, unselected group of 161 children and adolescents with Type 1 diabetes mellitus, treated mainly (81%) with multiple-dose insulin therapy. Patients and families were asked to write in the diary all the symptomatic episodes in which blood glucose concentration proved to be < or =3 mmol l(-1) before treatment. Of the patients, 83 (52%) had a total of 287 hypoglycaemic episodes (0.6 attack per month per patient). The majority of the attacks, 221 (77%), were mild (patients > or =6 years able to treat themselves). Only two attacks were severe, resulting in coma and/or convulsion. The most common dominant symptoms were weakness (29%), tremor (20%), hunger (14%), and drowsiness (12%). Of all the dominant symptoms, 39% were classified as autonomic, 20% neuroglycopenic, and 41% non-specific. In children under 6 years, autonomic symptoms were less common than in adolescents 15 years or over (34% vs 57%, p = 0.01). In conclusion, the incidence of documented symptomatic hypoglycaemia was low. The symptoms were more often neuroglycopenic or non-specific than autonomic, especially in young children.
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PMID:Documented symptomatic hypoglycaemia in children and adolescents using multiple daily insulin injection therapy. 963 24

We have investigated the potential for the human brain to use lipid fuels during acute hypoglycemia. Nine healthy male subjects underwent hyperinsulinemic (1.5 mU/kg x min) stepped hypoglycemic clamps on two occasions, infusing Intralipid (20%) and heparin (0.1 U/kg x min) on one occasion only (ILH), with an identical study without infusion of ILH acting as a control. Five subjects also underwent euglycemic clamping with Intralipid/heparin infusion. During hypoglycemia, ILH raised circulating levels of nonesterified fatty acids, glycerol, and beta-hydroxybutyrate, although the latter did not rise until after the onset of counterregulation. With ILH, epinephrine responses [area under the curve (AUC), 127.9 +/- 31.7 vs. 175.1 +/- 27.4 nmol/L x 180 min; P = 0.03] and GH responses (AUC, 260 +/- 91 vs. 1009 +/- 150, P < 0.01) were reduced and delayed (glucose thresholds, 2.8 +/- 0.04 vs. 3.0 +/- 0.1 mmol/L; P = 0.04), with a trend toward reduced cortisol responses. Similarly, hypoglycemic symptom scores were diminished during ILH (AUC, 647 +/- 162 vs. 1222 +/- 874; P = 0.03). However, there was no significant effect on the deterioration in four-choice reaction time, one measure of cognitive deterioration [glucose thresholds, 2.6 +/- 0.1 vs. 2.7 +/- 0.1 mmol/L, ILH vs. control (P = 0.75); AUC, 1420 +/- 710 vs. 2250 +/- 1080 ms/min (P = 0.59)]. During euglycemic clamping with Intralipid/heparin infusion studies, there was no rise in hormones, four-choice reaction time, or symptoms other than hunger and tiredness. Both nonesterified fatty acids and glycerol can penetrate the mammalian brain and be metabolized. Raised levels were able to reduce neurohumoral responses to hypoglycemia, but could not protect cognitive function. This suggests that regional differences exist in human brain metabolism between glucose-sensing and cognitive areas of brain, which may be important in the understanding of the mechanisms of glucose sensing and in the genesis of hypoglycemia unawareness in insulin-dependent diabetes.
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PMID:Reduced counterregulation during hypoglycemia with raised circulating nonglucose lipid substrates: evidence for regional differences in metabolic capacity in the human brain? 970 75

Hypoglycaemic events are frequent complications of insulin-dependent diabetes mellitus in children. The signs and symptoms referred to by young children can be difficult to understand and often seem to be different from those described by their parents. We analysed the hypoglycaemic symptoms described by a group of patients and their parents. We studied 40 pairs consisting of a parent and a diabetic child by using a structured questionnaire with 27 items concerning different symptoms of hypoglycaemia. The mean+/-SD age of the children was 10.4+/-2.4 years, with duration of disease 6.2+/-2.1 years and their HbA1c was 8.2 2.0%. For the statistical analysis we used the principal component analysis. All the children followed a multiple injection regimen. The frequency and intensity of the hypoglycaemic signs described by patients and parents were similar both for neuroglycopenic (uncoordination, confusion, odd behaviour, dizziness) and autonomic symptoms (trembling, sweating, pounding heart, hunger). Moreover, our questionnaire showed a high frequency of behavioural changes. In conclusion, from the analysis of the questionnaires collected, we found that both parents and children gave almost the same score to the symptoms observed. This means that there is a concordance between the symptoms reported by the children and those reported by their parents.
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PMID:Hypoglycaemic symptoms described by diabetic children and their parents. 974 59

The patient, a 24-year-old man, had suffered from hunger, sweating, tachycardia and palpitation for three years. He was diagnosed as having Graves' disease (GD) and treated with methimazole (MMI) for 3 months. He noted that palpitation and perspiration seemed to particularly occur when he was hungry, and thus he was examined to determine whether these symptoms were caused by hypoglycemia. As a markedly elevated immunoreactive insulin level and the presence of insulin antibody in serum were found, he was diagnosed as having insulin autoimmune syndrome (IAS). HLA typing revealed the patient to be positive for group Bw62/Cw4/DR4, which is reportedly a specific HLA type in MMI-treated euthyoroid GD patients with IAS. In spite of the continuation of MMI treatment, the % binding of IRI decreased and the hypoglycemic episode disappeared. In contrast to the previously reported MMI induced IAS in GD cases, MMI is unlikely to have exacerbated IAS in the present case, although his HLA combination is identical to that of the previous cases.
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PMID:Remission of insulin autoimmune syndrome in a patient with Grave's disease by treatment with methimazole. 1041 53

Ultimately traceable to neural glucose deprivation, symptoms of hypoglycemia include neurogenic (autonomic) and neuroglycopenic symptoms. Neurogenic symptoms (tremulousness, palpitations, anxiety, sweating, hunger, paresthesias) are the results of the perception of physiologic changes caused by the autonomic nervous system's response to hypoglycemia. Neuroglycopenic symptoms (confusion, sensation of warmth, weakness or fatigue, severe cognitive failure, seizure, coma) are the results of brain glucose deprivation itself. Glycemic thresholds for symptoms of hypoglycemia shift to lower plasma glucose concentrations following recent episodes of hypoglycemia, leading to the syndrome of hypoglycemia unawareness--loss of the warning symptoms of developing hypoglycemia. Thus, patients with recurrent hypoglycemia (e.g., those with tightly controlled diabetes or with an insulinoma) often tolerate abnormally low plasma glucose concentrations without symptoms.
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PMID:Symptoms of hypoglycemia, thresholds for their occurrence, and hypoglycemia unawareness. 1050 Sep 27

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.
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PMID:Hypothalamic orexin expression: modulation by blood glucose and feeding. 1053 45

The hypothalamus is the focus of many peripheral signals and neural pathways that control energy homeostasis and body weight. Emphasis has moved away from anatomical concepts of 'feeding' and 'satiety' centres to the specific neurotransmitters that modulate feeding behaviour and energy expenditure. We have chosen three examples to illustrate the physiological roles of hypothalamic neurotransmitters and their potential as targets for the development of new drugs to treat obesity and other nutritional disorders. Neuropeptide Y (NPY) is expressed by neurones of the hypothalamic arcuate nucleus (ARC) that project to important appetite-regulating nuclei, including the paraventricular nucleus (PVN). NPY injected into the PVN is the most potent central appetite stimulant known, and also inhibits thermogenesis; repeated administration rapidly induces obesity. The ARC NPY neurones are stimulated by starvation, probably mediated by falls in circulating leptin and insulin (which both inhibit these neurones), and contribute to the increased hunger in this and other conditions of energy deficit. They therefore act homeostatically to correct negative energy balance. ARC NPY neurones also mediate hyperphagia and obesity in the ob/ob and db/db mice and fa/fa rat, in which leptin inhibition is lost through mutations affecting leptin or its receptor. Antagonists of the Y5 receptor (currently thought to be the NPY 'feeding' receptor) have anti-obesity effects. Melanocortin-4 receptors (MC4-R) are expressed in various hypothalamic regions, including the ventromedial nucleus and ARC. Activation of MC4-R by agonists such as alpha-melanocyte-stimulating hormone (a cleavage product of pro-opiomelanocortin which is expressed in ARC neurones) inhibits feeding and causes weight loss. Conversely, MC4-R antagonists such as 'agouti' protein and agouti gene-related peptide (AGRP) stimulate feeding and cause obesity. Ectopic expression of agouti in the hypothalamus leads to obesity in the AVY mouse, while AGRP is co-expressed by NPY neurones in the ARC. Synthetic MC4-R agonists may ultimately find use as anti-obesity drugs in human subjects Orexins-A and -B, derived from prepro-orexin, are expressed in specific neurones of the lateral hypothalamic area (LHA). Orexin-A injected centrally stimulates eating and prepro-orexin mRNA is up regulated by fasting and hypoglycaemia. The LHA is important in receiving sensory signals from the gut and liver, and in sensing glucose, and orexin neurones may be involved in stimulating feeding in response to falls in plasma glucose.
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PMID:The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box. 1099 54


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