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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin, gastrin-releasing peptide (GRP) and gastrin were measured in the stomach of rats with streptozotocin-induced diabetes, insulinoma-bearing rats and their respective controls. Rats injected with streptozotocin exhibited hyperphagia, insulinopenia and severe hyperglycemia. Stomach weights, and the concentrations and total amounts of GRP and gastrin in the stomach, were similar to nondiabetic control rats. The concentration of somatostatin in the stomach of diabetic rats was 25% greater, but the total stomach content of somatostatin was similar to that of control rats. Insulinoma-bearing rats exhibited hyperphagia, hyperinsulinemia and hypoglycemia. Concentrations of GRP and gastrin in the stomach were 72% and 19% lower, respectively, than in control rats. Despite 45% greater stomach weight, the total stomach content of GRP was 61% lower. Stomach concentrations of somatostatin, and total stomach contents of somatostatin and gastrin, were similar in insulinoma-bearing and control rats. The results demonstrate abnormalities in the stomach concentrations of regulatory peptides in rats with diabetes and insulinoma. These abnormalities are not attributable to changes in food intake alone, suggesting specific effects of these metabolic diseases on gastric regulatory peptides and gastric function.
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PMID:Somatostatin, gastrin-releasing peptide and gastrin in the stomach of rats with streptozotocin-induced diabetes and insulinoma. 167 27

28 obese women were investigated in the course of the 21st (A) and 30th (B) week of pregnancy. Increased serum levels of GH, T4 and T3 were found in both samples of blood (A and B), while serum insulin, cholesterol and triacylglycerols were increased only at time B. It was suggested that the similar increase of GH, T4 and T3 at time A and B was due to pregnancy because the level of these hormones is usually not increased in non-pregnant obese women, while hyperinsulinemia and often increased values of cholesterol and triacylglycerols are a common finding in non-pregnant obesity. This presumption was confirmed only partially--body weight and the skin folds correlated only with insulin and T3, while GH, cortisol, T4, cholesterol and triacylglycerols correlated only exceptionally. High levels of insulin and T3 may be due to overeating.
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PMID:[Pregnancy and obesity. II. Hormonal and metabolic changes]. 191 57

Hypothalamic concentrations of neuropeptide Y (NPY), a potent central appetite stimulant, increase dramatically in food-restricted and insulin-deficient diabetic rats. This suggest that NPY may drive hyperphagia in these conditions, which are characterized by weight loss and insulin deficiency. To test the hypothesis that insulin deficiency and weight loss are specific stimuli to hypothalamic NPY, we measured NPY concentrations in individual hypothalamic regions in rats with hyperphagia caused by insulin-induced hypoglycemia. Groups of 8 male Wistar rats were injected with ultralente insulin (20-60 U/kg) to induce either acute hypoglycemia (7 h after a single injection) or chronic hypoglycemia (8 days with daily injections). In hypoglycemic rats, plasma insulin concentrations were increased 6- to 7-fold compared with saline-injected controls; food intake was significantly increased with acute and chronic hypoglycemia and weight gain was significantly increased in the chronically hypoglycemic group. NPY concentrations were measured by radioimmunoassay in 8 hypothalamic regions microdissected from fresh brain slices. NPY concentrations were not increased in any region in either acute or chronic hypoglycemia. NPY therefore seems unlikely to mediate hyperphagia in hyperinsulinemia-induced hypoglycemia, supporting the hypothesis that weight loss is a specific stimulus to hypothalamic NPY and that insulin deficiency may be the metabolic signal responsible.
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PMID:Unchanged hypothalamic neuropeptide Y concentrations in hyperphagic, hypoglycemic rats: evidence for specific metabolic regulation of hypothalamic NPY. 192 23

This study was performed to investigate the consequences of developing obesity on glucose homeostasis in animals showing hyperphagia plus vagal hyperinsulinemia and rats that were normophagic and hyperinsulinemic. Male rats were lesioned in the ventromedial hypothalamus (VMH) and kept either under ad libitum or absolute (oral or intragastrical) pair-feeding conditions for 4 weeks. Hyperphagic rats, as well as normophagic VMH rats, became obese, but only ad lib-fed obese rats displayed glucose intolerance to intravenous (IV) glucose infusions. Orally pair-fed VMH rats also showed normal oral and intragastric glucose tolerance, but in intragastrically fed VMH animals and controls, oral and intragastric glucose tolerance was decreased. These results indicate that (1) obesity as a consequence of VMH lesions is not dependent on hyperphagia, confirming earlier reports, and also independent of the ingestion of bulk meals. (2) beta-cell release of insulin to IV glucose infusion is not sufficient when hyperphagia and vagally mediated hyperinsulinemia coincide, and is therefore dependent on several factors; and (3) oral glucose intolerance develops when preabsorptive reflexes are blunted, irrespective of whether the animals were hyperinsulinemic or not.
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PMID:Hyperinsulinemia and glucose tolerance in obese rats with lesions of the ventromedial hypothalamus: dependence on food intake and route of administration. 194 35

Insulin levels in a 7-year-old boy with hyperphagia and obesity following an episode of meningoencephalitis were studied sequentially during the course of progressive weight gain. High fasting insulin levels (1183 pmol/L) and strikingly high insulin release in response to glucose (7892 pmol/L) were found within weeks of the onset of the illness. The abnormality in insulin secretion occurred prior to the marked weight gain. Hyperinsulinemia was not accompanied by hypoglycemia. Early hyperinsulinemia may be a primary event in the development of hyperphagia and obesity following hypothalamic injury.
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PMID:Hypothalamic or central obesity is associated with an early rise in plasma insulin concentration. 201 20

Two-month hyperphagia after injury inflicted to the ventromedial hypothalamus in rats led to the development of marked obesity in an essential increase of the content of immunoreactive insulin, glucagon, and C-peptide in the blood. Increase of excessive body weight was attended by gradual diminution of the organisms sensitivity to exogenous insulin given in a dose of 0.03 U/100 g and maintenance of normal sensitivity to 0.1 U/100 g of exogenous insulin. It is most likely, therefore, that despite the increased function of the pancreatic islets and hyperinsulinemia, glucose tolerance decreased significantly due to diminished sensitivity of the peripheral tissues to insulin.
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PMID:[Insulin sensitivity of the body in experimental hypothalamic obesity]. 208 61

Adrenalectomy arrests the development of obesity in ob/ob mice fed a high-starch diet and housed at a normal room temperature (20-25 degrees C) partly by stimulating the low thermogenic activity of brown adipose tissue (BAT). The present study was undertaken to determine if adrenalectomy would also lower energy retention and stimulate BAT metabolism in ob/ob mice housed in a warm environment (35 degrees C) where BAT thermoregulatory heat production is not needed. Adrenalectomy prevented hyperphagia and hyperinsulinemia and lowered the efficiency of energy retention in ob/ob mice housed at 35 degrees C, which is comparable to results obtained at 20-25 degrees C. Sympathetic nervous system stimulation of BAT (interscapular and subscapular depots) assessed by norepinephrine turnover was increased in adrenalectomized ob/ob mice. Thermogenic activity of BAT in adrenalectomized ob/ob mice (as assessed by GDP binding to isolated BAT mitochondria, GDP-inhibitable acetate-induced BAT mitochondrial swelling, and Mg2(/)-activated GDP binding to BAT mitochondria) was not elevated when results were expressed per milligram of mitochondrial protein but was elevated approximately 65% when expressed per interscapular and subscapular depots because adrenalectomy increased BAT mitochondrial mass. Adrenalectomy lowers the efficiency of energy retention and stimulates BAT metabolism even when ob/ob mice are housed in a warm environment.
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PMID:Adrenalectomy increases brown adipose tissue metabolism in ob/ob mice housed at 35 degrees C. 216

The significance of portal venous drainage after whole-pancreas transplantation both for metabolic control and development of diabetic nephropathy was investigated. Streptozotocin-diabetic inbred LEW rats received a duct-ligated pancreas graft with either systemic or portal venous drainage and were followed for up to one year. Normal and untreated diabetic rats (n=18 in each group) served as controls. Irrespective of the route of venous drainage pancreas transplants normalized the diabetic polyuria, polyphagia, and polydipsia. Growth rates and general health did not differ from normal rats. Pancreas transplantation with portal venous drainage furthermore normalized nonfasting blood glucose and peripheral insulin levels, and intravenous glucose tolerance. Pancreas transplantation with systemic venous drainage, however, was associated with peripheral hyperinsulinemia, slightly elevated nonfasting blood glucose levels, and supranormal K-values in intravenous glucose tolerance tests. Though portal venous drainage was associated with better metabolic control than systemic venous drainage, both techniques of pancreas transplantation proved equally effective to prevent the development of diabetic glomerular membrane thickening determined 6 and 12 months posttransplant.
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PMID:Significance of portal venous drainage after whole-organ pancreas transplantation for endocrine graft function and prevention of diabetic nephropathy. 240 87

1. Sprague-Dawley rats were injected for 16 d with long-acting insulin, and energy balance was calculated using the comparative carcass technique. Two experiments were carried out with females (starting weights 150 and 90 g respectively), and one with males (starting weight 150 g). In a fourth experiment, cytochrome c oxidase (EC 1.9.3.1) activity was measured as an indicator of the capacity for substrate oxidation. 2. Insulin increased weight gain by up to 57% (P less than 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P less than 0.01 for all studies). The excess weight gained by the insulin-treated rats was predominantly due to fat deposition. 3. Energy expenditure, calculated as the difference between metabolizable intake and carcass energy gain, was expressed on a whole-body basis, or relative to either metabolic body size (kg body-weight0.75) or fat-free mass. Insulin consistently raised energy expenditure, regardless of the method of expression, but this change reached statistical significance in only two of the nine comparisons. 4. Cytochrome c oxidase activity was not affected by insulin treatment in either interscapular brown adipose tissue or gastrocnemius muscle. In liver, total enzyme activity (U/tissue) was increased from 2928 (SE 162) in the controls to 3940 (SE 294) in the treated group (P less than 0.02), but specific activity (U/mg protein) was unchanged. 5. It is concluded that, despite causing substantial hyperphagia, insulin treatment only slightly increases energy expenditure in rats. The costs of increased tissue deposition may account for this change.
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PMID:Energy balance in rats given chronic hormone treatment. 1. Effects of long-acting insulin. 254 25

The influence of experimental hyperinsulinemia on energy intake, energy expenditure, and body composition was investigated in rats treated chronically with high doses of insulin. Energy balance studies, each of 2-wk duration, were conducted with two different long-acting insulins (Protamine and Monotard), administered in the morning (IM), the late afternoon (IA), or both (IMA) and in animals of three different ages, namely in 4-, 8-, and 12-wk-old rats. The results indicate that the level of hyperphagia induced by insulin was markedly influenced by the type of long-acting insulin (P less than 0.001; Protamine greater than Monotard), by age (P less than 0.001; 12 greater than 8 greater than 4 wk), as well as by the timing of insulin administration (P less than 0.002, IMA greater than IM or IA). Body protein deposition was unaltered, but body fat and energy expenditure increased in parallel to the level of hyperphagia. Regression analysis shows a strong linear correlation (r = 0.963) between the change in energy expenditure and the change in energy intake in response to insulin and indicates that approximately 50% of the excess calories consumed was dissipated as heat. In the absence of hyperphagia, however, insulin administration had no effect on energy expenditure nor on energy partitioning. Similarly, the influence of altered meal pattern, induced by administering insulin at different times of the day, was also found to have no impact on energy expenditure. The current investigations therefore refute the notion that high doses of insulin via hyperinsulinemia and/or altered meal pattern have an inhibitory influence on whole body thermogenesis. In contrast, our data demonstrate that the adaptive phenomenon that tends to minimize the accumulation of excess caloric intake, i.e., diet-induced thermogenesis, persists in the hyperinsulinemic state.
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PMID:Energy expenditure and diet-induced thermogenesis in presence and absence of hyperphagia induced by insulin. 267 50


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