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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 12 out of 51 maladjusted diabetics treated with insulin chronic insulin overdosage could be established as the reason. Increasing insulin requirements, avid hunger, profuse sweating, vertigo and emotional lability as well as grossly variable glucosuria are evidence of insulin overdosage. Treatment consists of low reduction of daily insulin dosage.
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PMID:[Chronic insulin overdosage in adult diabetics (author's transl)]. 699 84

We employed a delayed feeding paradigm to assess regional brain catecholamine changes associated with insulin-elicited glucoprivic feeding. This paradigm makes use of the recent discovery that glucoprivic challenges significantly enhance food intake even when food is withheld until other signs of glucoprivation have abated. Using this paradigm we attempted to temporally dissociate the neurochemical events associated with the ingestive response from other potentially confounding consequences of insulin or glucoprivation. We found a high degree of congruence between elevated hypothalamic norepinephrine (NE) turnover (estimated by the change in transmitter concentration after synthesis inhibition) and the persistence of hunger, both during and after apparent glucoprivation. In the absence of food, hypothalamic NE turnover was enhanced during insulin-induced glucoprivation and this increase persisted into the postglucoprivic period. A brief feeding bout, either during glucoprivation or postglucoprivically, rapidly normalized NE turnover rates. Moreover, brief access (30 min) to a limited quantity of food (2.5 g) during glucoprivation abolished both the elevated turnover and the feeding response otherwise observed postglucoprivically. Turnover of catecholamines in the telencephalon was also enhanced after insulin, but the increased activity did not persist into the postglucoprivic period and, in addition, was not altered in any consistent manner by food intake. These findings strengthen the view that hypothalamic NE neurons are involved in the mediation of glucoprivic feeding.
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PMID:Insulin-induced elevation of hypothalamic norepinephrine turnover persists after glucorestoration unless feeding occurs. 701 42

Physiological changes accompanying a period of voluntary hypophagia in male Sprague-Dawley rats after insulin-induced hyperphagia and body weight gain were investigated. Postinsulin hypophagia was manifested as a reduction in meal duration diurnally and nocturnally (Geary et al., Behav. Neural Biol. 31: 435-442, 1981). Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats, suggesting a postabsorptive mechanism controlled the hypophagia. Basal blood glucose and plasma nonesterified fatty acids, 3-hydroxybutyrate, glycerol, and some amino acids were elevated during hypophagia, while liver glycogen content was reduced. Hypophagic rats' arteriovenous blood glucose differences and glucose oxidation rates, however, were not different from controls. After nutrient repletion blood glucose and plasma glycerol remained elevated in hypophagic rats in comparison to controls, while differences in other plasma metabolites were reduced. Liver glycogen accumulated faster in hypophagic rats. These data were related to the lipostatic and other hypotheses how energy balance status affects hunger and satiety.
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PMID:Blood metabolites and feeding during postinsulin hypophagia. 705 64

To investigate the relative potency of short-term control mechanisms for carbohydrate satiety, ten fasted, healthy male volunteers consumed a 250-ml, 30% glucose drink with and without the addition of guar gum (2%). Gastric emptying, hunger and fullness ratings and blood glucose and insulin levels were monitored over the following 3 h and energy intake was recorded from a test meal given 3.5 h after the drinks. The addition of the guar gum to the glucose drink lowered both postprandial glucose and insulin levels over the following 2 h. This was associated with a reduction in the ratings for hunger and desire to eat and an increase in ratings for fullness and satiety, but energy intake from the test meal was unchanged. There was no difference between values for the half time for gastric emptying for the two drinks. The short-term increase in satiety and decrease in hunger seen when glucose absorption was slowed with guar gum is unlikely to be explained by the reduction in postprandial glycaemia or differences in gastric emptying, and instead may implicate increased contact of the carbohydrate with receptors in the small intestine and consequent enhanced release of putative satiety peptides.
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PMID:The effect on hunger and satiety of slowing the absorption of glucose: relationship with gastric emptying and postprandial blood glucose and insulin responses. 749 29

The efficacy of the new intestinal alpha-glucosidase inhibitor, miglitol, and glibenclamide were compared in a 6-month double-blind controlled protocol involving 100 non-insulin dependent diabetic patients under diet alone. HbA1c levels (initially between 7 and 11%) were reduced (p < 0.05): -0.78 +/- 0.21% after miglitol and -1.18 +/- 0.20% after glibenclamide. The difference between the two treatments was not significant, although glibenclamide appeared to be more active than miglitol at 8 (p = 0.002) and 16 weeks (p = 0.01) but not at 24 weeks. Fasting glycaemia decreased after miglitol (8.7 +/- 0.3 vs 9.6 +/- 0.3 mmol/l, p = 0.005) and after glibenclamide (8.0 +/- 0.3 vs 9.1 +/- 0.3, p = 0.007). After miglitol, a decrease was noted after breakfast (p < 0.001) and lunch (p < 0.001). The same was true for glibenclamide (p = 0.004 and p < 0.001 respectively). A significant reduction in glucose incremental area during a standard meal test was noted at the end of miglitol (p = 0.008) or glibenclamide treatment (p = 0.04). Subgroups of nonresponders to both treatments were identified (10/49 with miglitol, 9/47 with glibenclamide). Side effects were recorded in 10 patients treated with miglitol (flatulence and meteorism, diarrhoea, 1 discontinued therapy) and in 10 treated with glibenclamide (asthenia, sensation of hunger). This study indicates that miglitol is suitable for initial application in diet-resistant Type 2 diabetic patients, providing, a persistent effect and acceptable side effects.
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PMID:Comparison of miglitol and glibenclamide in diet-treated type 2 diabetic patients. 755 6

Anorexia nervosa (AN) is associated with a paradoxical reduction in hunger ratings following 2-deoxy-D-glucose (2DG) induced glucose insufficiency. Because of the relationship between exercise and AN, there is interest in the weight-loss phenomenon produced by exercise in food restricted rats. This investigation determined if the weight-loss phenomenon is associated with a paradoxical suppression of food intake following 2DG and if the effect is related to reductions in prevailing glucose and insulin levels. Weight-matched, normal-weight exercised and normal-weight unexercised rats served as controls. As predicted, 2DG reduced food intake in animals subjected to the phenomenon (1.5 h/day food access and 22.5 h/day running wheel access). This effect was related to reductions in plasma glucose and insulin under the conditions that prevailed at the time of injection. Since these changes also occurred in weight-matched controls, they were attributed to the general effects of weight loss. A situational specificity for the "anorexia" of the weight-loss syndrome was also demonstrated. Finally, the strengths and weaknesses of the phenomenon as a model of AN were considered.
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PMID:Exercise in food-restricted rats produces 2DG feeding and metabolic abnormalities similar to anorexia nervosa. 787 8

1. Insulin-induced hypoglycaemia is characterized by an autonomic disturbance which produces some of the symptoms of hypoglycaemia. How an additional autonomic stress like postural change may alter physiological responses and symptoms of hypoglycaemia is not known. In 10 healthy male subjects (mean age 24 years) we observed physiological and symptomatic responses to postural change during acute (20 min) and prolonged (60 min) hyperinsulinaemic (60 m-units min-1 m-2) hypoglycaemia (2.5 mmol/l) and euglycaemia (4.5 mmol/l), and placebo control (saline). 2. In all studies standing increased plasma catecholamines (adrenaline, P < 0.001; noradrenaline, P < 0.0001), blood pressure (P < 0.0001) and heart rate (P < 0.0001). Catecholamine responses to standing were augmented by acute hypoglycaemia (adrenaline, P < 0.005; noradrenaline, P < 0.01), but less so by prolonged hypoglycaemia (adrenaline, P < 0.05; noradrenaline, P < 0.05). Supine heart rate was higher before standing during prolonged hypoglycaemia (P < 0.05), but did not increase as much on standing when compared with acute hypoglycaemia and prolonged euglycaemia. 3. During acute hypoglycaemia, autonomic symptoms increased on standing, but during prolonged hypoglycaemia, in the presence of generally higher symptom scores, standing had no effect. Autonomic symptoms, with the exception of hunger, tended to decrease with time (P < 0.05) during prolonged hypoglycaemia. 4. To conclude, posture does modify the catecholamine and symptomatic responses to hypoglycaemia, but this effect is dependent on the duration of hypoglycaemia. Hypoglycaemia and hyperinsulinaemia had little or no effect on the cardiovascular responses to changing posture.
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PMID:Physiological and symptomatic responses to postural change in non-diabetic subjects during hypoglycaemia. 792 64

It is proposed that chronic hyperinsulinemia is largely responsible for hunger, cravings and weight gain observed in many obese. This form of obesity can be treated by decreasing frequency of daily intake of carbohydrates to one well-balance meal each day and allowing for additional meals that are low in fat, low carbohydrates and high fiber. Animal experimentation and epidemiological evidence support the role of chronic hyperinsulinemia as a major factor in obesity and accounts for the frequent failures of diet and behavioral modification programs. Chronic hyperinsulinemia upsets metabolic balances and favors anabolic metabolism; fosters carbohydrate cravings; promotes insulin resistance which further promotes anabolic metabolism; and insulin resistance in turn exacerbates chronic hyperinsulinemia. This vicious cycle maintains excess weight and defeats diet and behavioral modification attempts to treat obesity. An eating program focused on reduction of chronic hyperinsulinemia coupled with appropriate exercise and behavior modification can successfully and permanently bring down cravings, hunger and body weight.
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PMID:Hyperinsulinemic obesity and carbohydrate addiction: the missing link is the carbohydrate frequency factor. 793 72

Suspected postprandial (reactive or idiopathic) hypoglycemia is characterized by predominantly adrenergic symptoms appearing after meals rich in carbohydrates and by their rare association with low blood glucose level (< 2.77 mmol/L). We studied heart rate, blood pressure, plasma insulin, C-peptide, and catecholamine responses during a 5-h oral glucose tolerance test in eight patients with suspected postprandial hypoglycemia and eight age-, sex-, and body mass index-matched healthy controls. We also evaluated beta-adrenergic sensitivity by using the isoproterenol sensitivity test. Psychological profile was assessed by the Symptom Checklist (SCL-90R) self-report symptom inventory. Patients with suspected postprandial hypoglycemia had higher beta-adrenergic sensitivity (defined as the dose of isoproterenol required to increase the resting heart rate by 25 beats/min) than controls (mean +/- SEM, 0.8 +/- 0.13 vs. 1.86 +/- 0.25 microgram isoproterenol; P = 0.002). After administration of glucose (75 g) blood glucose, plasma C-peptide, plasma epinephrine, and plasma norepinephrine responses were identical in the two groups, but plasma insulin was higher in the patients (group effect, P = 0.02; group by time interaction, P = 0.0001). Both heart rate and systolic blood pressure were significantly higher (but remained in the normal range) after glucose administration in patients with suspected postprandial hypoglycemia than in controls (group by time interactions, P = 0.004 and 0.0007, respectively). After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger. Analysis of the SCL-90R questionnaire revealed that patients had emotional distress and significantly higher anxiety, somatization, depression, and obsessive-compulsive scores than controls. We may conclude that patients with suspected postprandial hypoglycemia have normal glucose tolerance, increased beta-adrenergic sensitivity, and emotional distress.
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PMID:Suspected postprandial hypoglycemia is associated with beta-adrenergic hypersensitivity and emotional distress. 796 39

In general, obesity is a state of high energy stores, high energy intake, and high energy expenditure. The high energy expenditure is largely due to the increased fat-free mass. The failure to find a positive relationship between reported energy intake and body size reflects a greater under-reporting of calorie intake among obese individuals. Obesity, therefore, develops as a consequence of a chronic imbalance between intake and expenditure, although the cause of this is not apparent from the energy balance equation. However, this equation can be dissected into its component nutrient balance equations because net de novo lipogenesis is negligible in free-living humans. Fat calories are handled very differently from non-fat calories. Non-fat nutrient oxidation rates rise and fall to match the fluctuations in non-fat intake so that non-fat calorie balance is actively maintained. In contrast, changes in fat intake do not acutely affect fat oxidation but are matched by changes in storage. Therefore, within the fat balance equation there is ample scope for a chronic imbalance between fat intake and oxidation. Also, there is some evidence that carbohydrate balance may be an important signal for hunger and satiety. These concepts imply that, under free-living, ad libitum eating conditions, changes in nutrient intake composition (e.g. an increased proportion of fat in the diet) or changes in nutrient oxidation composition (e.g. a decrease in the proportion of fat oxidized) will lead to body weight change (in these cases, to weight gain). Considering obesity as a consequence of normal physiology (with its normal variation between individuals) in a 'pathological' environment (high fat diet, low exercise) offers an important perspective for explaining the interpopulation and interindividual differences in obesity and for formulating treatment and prevention options. Low energy expenditure (relative to body size), high respiratory quotient and insulin sensitivity have been shown to be predictors of weight gain, although upon gaining weight these metabolic factors tend to 'normalize'. Metabolic responses to underfeeding or overfeeding are largely predictable from the changes in calorie intake and changes in body composition, but some adaptive changes may occur.
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PMID:Energy and macronutrient metabolism. 798 Mar 46


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