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

A case of a patient with hyperinsulinism due to insulinoma associated with neurological and psychiatric disturbances including EEG alterations is reported. The hunger test as well as the i.v. tolbutamid test proved to be of diagnostic importance. In addition, the electroencephalographic studies combined with blood sugar analyses before and after 50 g glucose, orally, showed a reversibility of the EEG alterations together with normalization of the blood surgar levels. These results point to the possibility of differentiating biochemical from structural cerebral lesions associated with hyperinsulinism.
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PMID:[Hyperinsulinism. Neurological and psychiatric aspects (author's transl)]. 5 30

The clinical picture of organic hyperinsulinism is presented with reference to experience in 46 operated patients. For the recognition of disease, a careful history is a decisive contribution. The hunger test showed a characteristic hypoglycemic reaction in 100%; the tolbutamide test gave a positive result in 92%. Insulinomas could be localized angiographically in 71%; in one patient this could only be done with an ERCT. The treatment of choice is operation as soon as possible. If possible, enucleation is to be given preference over pancreas resection because of the low complication rate. A search for ectopic (2%) and multiple (12%) adenomas is important. A cure was achieved in 76% of all those operated on. The hospital mortality was about 4%.
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PMID:[Clinical aspects, diagnosis and treatment of organic hyperinsulinism. Experience with 46 operated patients (author's transl)]. 20 79

The hypoglycemias caused by organic hyperinsulinism are predominantly manifested by means of neuropsychiatric disorders. They include losses of consciousness and seizures occurring in the period of hunger. The method of choice in the treatment of this disorder is surgical treatment of pancreatic neoplasms. This implies the need of early diagnostic procedure.
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PMID:[Organic hyperinsulinism as a diagnostic problem in neuropsychiatric practice]. 263 87

An hyperglycaemic metabolic state disappeared and spontaneous hypoglycaemia occurred in a 58-year-old woman with non-insulin-dependent obese type II diabetes. Abnormal absence of the hunger response with provoked hypoglycaemia, increased serum insulin concentrations and reduced blood glucose/insulin ratio led to the diagnosis of pathological hyperinsulinism, which was found to be due to an insulinoma of the tail of the pancreas. After its excision the patient's carbohydrate metabolism returned to a mild type II diabetic state and there were no further hypoglycaemic attacks.
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PMID:[Hypoglycemia caused by insulinoma in diabetes mellitus]. 284 54

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.
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PMID:Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition? 305 64

The paper reviews studies considering whether hyperinsulinemia, and its resultant effects on adipose tissue mass, can alter perceived hunger, taste, and food consumption. It also describes work addressing the reciprocal question of whether cues associated with food can affect insulin response. Specifically, four general categories of studies are presented. First, studies considering the causes and physiological consequences of chronic hyperinsulinemia are reviewed. Second, work investigating environmental and cognitive influences on insulin secretion are described. These show that high acute levels of insulin can be produced by simply seeing and thinking about food and that individuals showing this response show a greater tendency toward weight gain in a food-abundant environment. Third, studies are covered in which direct manipulations of insulin level, controlling for blood glucose, are performed. These experiments show that elevations in insulin produce increased hunger, heightened perceived pleasantness of sweet taste, and increased food intake. Finally, a study is described that considers how different insulin levels, produced by the type of food ingested, may affect subsequent food intake. Together, these studies show that "overeating" is caused by a complex feedback system of environmental, behavioral, and biological factors.
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PMID:Insulin levels, hunger, and food intake: an example of feedback loops in body weight regulation. 389 1

Four experimental groups of human subjects, in whom plasma glucose and insulin were independently raised or lowered, were tested for perceptions of hunger, taste, bodily state, and food intake. The data showed that hyperinsulinemia, unrelated to change in plasma glucose concentration, resulted in increased hunger, heightened palatability of sucrose or sweetness, and greater food intake.
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PMID:Effect of insulin and glucose on feeding behavior. 389 69

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

Hyperglycemia may influence satiety. One mechanism by which glucose could influence food intake is hyperinsulinemia. Therefore, we investigated the short-term effects of acute hyperglycemia and euglycemic hyperinsulinemia on satiety. Six healthy volunteers (aged 20 to 26 years) were studied for 240 minutes on three separate occasions in random order during (1) intravenous (i.v.) saline (control), (2) acute hyperglycemic hyperinsulinemia (HG) with plasma glucose at 15 mmol/L, and (3) euglycemic hyperinsulinemia (HI) with plasma insulin at 80 mU/L and glucose at 4 to 5 mmol/L. Subjective criteria for appetite like the wish to eat, prospective feeding intentions ("How much food do you think you can eat?"), and feelings of hunger and fullness were scored on a 100-mm visual analog scale (VAS) at 30-minute intervals. Appetite was also measured every 60 minutes with the use of a food selection list (FSL). Appetite (prospective feeding intentions, feelings of hunger, and the wish to eat) gradually increased over basal levels during control conditions and HI. In contrast, prospective feeding intentions and feelings of hunger gradually decreased during HG and were significantly (P < .05) reduced versus basal and control levels during the last hour of the experiment. The wish to eat followed the same pattern. Feelings of fullness did not significantly change in all three experiments. Total food selection was not significantly decreased during HG, but the preference for fat-rich or carbohydrate-rich items tended to be reduced. The study suggests that in humans hyperglycemia induces satiety. This effect seems not to be mediated by insulin, since HI had no effect on appetite. However, a potentiating effect of endogenous insulin on the satiating effect of high blood glucose levels cannot be excluded.
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PMID:Effects of hyperglycemia and hyperinsulinemia on satiety in humans. 950 May 70

Ghrelin is a novel enteric hormone that stimulates growth hormone (GH), ACTH, and epinephrine; augments plasma glucose; and increases food intake by inducing the feeling of hunger. These characteristics make ghrelin a potential counterregulatory hormone. At present, it is not known whether ghrelin increases in response to insulin-induced hypoglycemia. To answer this question, we compared plasma ghrelin concentrations after a short-term insulin infusion that was allowed or not (euglycemic clamp) to cause hypoglycemia (2.7 +/- 0.2 mmol/l at 30 min) in five healthy volunteers. In both studies, plasma ghrelin concentrations decreased (P < 0.01) after insulin infusion (hypoglycemia by 14%, euglycemia by 22%), reached a nadir at 30 min, and returned to baseline at 60 min, without differences between the hypoglycemia and the euglycemia studies. Glucagon, cortisol, and GH increased in response to hypoglycemia despite the decreased ghrelin. There was a strong correlation (R(2) = 0.91, P < 0.002) between the insulin sensitivity of the subjects and the percentage suppression of ghrelin from baseline. These data demonstrate that ghrelin is not required for the hormonal defenses against insulin-induced hypoglycemia and that insulin can suppress ghrelin levels in healthy humans. These results raise the possibility that postprandial hyperinsulinemia is responsible for the reduction of plasma ghrelin that occurs during meal intake.
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PMID:Ghrelin is not necessary for adequate hormonal counterregulation of insulin-induced hypoglycemia. 1235 26


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