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

Dormice (Glis glis) undergo spontaneous cyclic changes in food intake and body weight. These infradian cycles with a periodicity of about 2 mo are endogenously controlled, since they persist in conditions of constant temperature and photoperiod. To evaluate the role of insulin as an effector of hyperphagia and fattening in dormice, experiments were conducted to study pancreatic function and adipose tissue metabolism during several phases of the infradian cycle. During the weight loss phase, peripheral insulin resistance occurs in the absence of hyperinsulinism. This resistance is not corrected by weight loss. Weight loss phase animals showed poor glucose tolerance and an impaired in vitro glucose-stimulated insulin secretion; these were not attributable to reduced pancreatic insulin content. Although basal glucose transport and basal, as well as insulin-stimulated, glucose utilization in isolated adipocytes were depressed during the weight loss phase, insulin-stimulated transport was significant. The data offer no evidence that insulin has a direct causal role in the development of spontaneous obesity in this species.
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PMID:Spontaneous obesity and weight loss: insulin action in the dormouse. 635 39

We studied insulin-like growth factors (IGF) I and II, prolactin, and the insulin response to arginine in 19 children with craniopharyngioma and documented growth hormone deficiency. Patients were divided into three groups according to their growth rate during the first postoperative year. Seven patients with excessive growth (Group A) had hyperinsulinism, normal IGF values, elevated basal prolactin levels, and a delayed thyrotropin response to thyrotropin-releasing hormone, which was compatible with hypothalamic lesions. In the six patients with normal growth (Group B), the insulin level was low; all other hormone values were similar to those of Group A. In the six patients with decreased growth (Group C), levels of IGF I, insulin, prolactin, and thyrotropin were low, indicating the presence of severe pituitary damage and explaining the failure to grow. Patients in all groups had low or undetectable basal levels of growth hormone. We conclude that in Group B, normal IGF permitted normal growth, and prolactin hypersecretion may have been responsible for normal IGF I values. Excessive growth in Group A may have been caused by hyperinsulinism associated with hyperphagia and obesity of hypothalamic origin.
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PMID:Insulin-like growth factors I and II, prolactin, and insulin in 19 growth hormone-deficient children with excessive, normal, or decreased longitudinal growth after operation for craniopharyngioma. 635 37

The relation of hyperinsulinemia to hyperphagia was examined in rats with lesions of the ventromedial hypothalamus (VMH). Plasma insulin and glucose levels were assayed after a 4-hr fast and 17 min after the initiation of a meal (6 ml of sweetened milk in 7 min) in animals with sham lesions, VMH animals maintained at preoperative body weight by food restriction, and VMH animals fed ad lib. Both VMH groups displayed basal and postabsorptive hyperinsulinemia, compared with the sham-operated control group, but insulin levels were greatest under the ad lib feeding condition. It is suggested that VMH hyperinsulinemia is due both to a primary effect of the lesion and to hyperphagia and that marked obesity can result in the absence of basal hyperinsulinemia as a result of hyperphagia with consequent postabsorptive hyperinsulinemia.
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PMID:Hyperinsulinemia in rats with ventromedial hypothalamic lesions: role of hyperphagia. 636 14

Much recent evidence suggests a dual and opposite action of insulin on food intake and body weight. Peripherally administered, long acting insulin stimulates weight gain and food intake. On the contrary intracerebroventricularly infused insulin decreases food intake and body weight. It has been suggested that the shift from the nocturnal hyperinsulinism and hyperphagia to the day-time hypoinsulinism and hypophagia depended on the action of insulin on the brain during the night. It has also been hypothesized that the absence of nocturnal hyperinsulinism due to fasting was partly responsible for the hyperphagia observed during the subsequent day-time. In the present experiment, insulin was infused intravenously at various low doses (0.01, 0.025, 0.05 U/hr) during a nocturnal fast. Its effects on the following diurnal free food intake were investigated. It was shown that the experimentally elevated plasma insulin induced a dose-dependent reduction in the day-time feeding response. It was concluded that this reduction is due to the chronic action on the brain of the high plasma insulin level induced by the infusion during the nocturnal fast.
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PMID:Insulin infusion during a nocturnal fast suppresses the subsequent day-time intake. 639 52

The immediate onset of hypermetabolism after a major burn dictates that nitrogen and calories be supplied as early as possible to such patients to prevent the well-documented catabolic state. However, intravenous hyperalimentation is not always possible, and enteral feeding is not usually attempted in the early resuscitative period. Twelve patients with major burns (40% to 70%) were fed nasoduodenally in the early postburn period with a new solution (3.5% Aminosyn, 25% Polycose, and appropriate additions of electrolytes and vitamins). All patients reached positive nitrogen balance in 9.8 +/- 2.3 days, tolerated the feeding extremely well, and had no distention or diarrhea. Metabolic assessment showed remarkable stability. The characteristic signs of hypermetabolism, such as hyperglycemia and hypoinsulinemia or hyperinsulinemia, were absent. Furthermore, there was no persistent neutrophilia or leukocytosis and there was a significant (p less than .01) decrease in the percentage of juvenile neutrophils and a significant (p less than 0.001) increase in absolute lymphocytes between days 0 and 14 of the study. These data indicate that early enteral feeding of Polycose-Aminosyn is safe and well tolerated, and that the small intestine absorbs nutrients readily in the early postburn period, leading to positive nitrogen balance, preventing loss of serum protein, assisting in the maintenance of normal carbohydrate metabolism, and restoring granulocytes and lymphocytes to normal ratios.
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PMID:Early enteral feeding of patients with major burns: prevention of catabolism. 644 Apr 66

The genetically diabetic mouse (db/db) exhibits hyperphagia, progressive weight gain, hyperglycemia, and hyperinsulinemia during the first few months of life during which time characteristic pathologic changes occur in several organ systems including the kidney. The extent to which long chain fatty acid oxidation (LCFAO) contributes to excessive gluconeogenesis and hyperglycemia in these animals in unknown. Therefore, the synthetic fatty acid analogue 2-tetradeclyglycidate (TDHA), a potent inhibitor of LCFAO, was given orally to db/db mice to evaluate its capacity to control the blood glucose and prevent their diabetic nephropathy. Five groups of diabetic mice (N = 6) were assigned to receive TDGA in a dose of 5, 10, and 25 mg/kg/day, vehicle (tragacanth), or nothing (control). TDGA had no observable effects on food intake or growth patterns. Drug-treated animals had significant lowering of fasting glucose at 0 and 4 h after dosing during the midportion of the study (2-6 wk). In the latter part of the study (wk 8-11), blood glucose 4 h after dosing was lowered in mice given 10 and 25 free fatty acids. Animals receiving TDGA 25 mg/kg/day exhibited significant inhibition of immunopathologic changes in the kidney. Heart weight was significantly increased in mice receiving TDGA 25 mg/kg/day, and the total amount of myocardial carnitine content was increased in all three drug-treated groups. Increased tissue deposition of lipid was not apparent on histologic examination of liver in drug-treated animals. Inhibition of long chain fat oxidation in the db/db mouse results in significant lowering of blood glucose, and decreased the renal immunopathologic features of diabetic nephropathy in this animal model.
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PMID:Metabolic control of prevention of nephropathy by 2-tetradecylglycidate in the diabetic mouse (db/db). 675 7

Adult female rats were adapted to a macronutrient self-selection regimen which allowed them ad libitum access to separate sources of protein, carbohydrate, and fat. The rats were then given either ventromedial hypothalamic (VMH) lesions, paraventricular hypothalamic (PVH) lesions, parasagittal knife cuts through the medial hypothalamus (CUT), or sham lesions and their macronutrient selection was studied for 60 days. Following surgery the VMH, PVH, and CUT rats overate and became obese compared with controls. The hyperphagias of the three groups were similar, although the CUT group gained more weight than did the PVH and VMH groups. All groups overate primarily by increasing their carbohydrate intake. The VMH and CUT groups, in addition, increased their protein intake such that their percent protein intake remain unchanged. The PVH group failed to increase its absolute protein intake and thus decreased its percent protein intake. Except for a transient increase, fat consumption was not affected by the lesions or knife cuts. During the 2nd postoperative mo (static phase) the total caloric intakes and the carbohydrate intakes of the VMH, PVH, and CUT groups returned to near normal levels. Rats with misplaced PVH lesions displayed minimal hyperphagia and failed to outgain controls but yet showed the same altered macronutrient selection pattern as did rats with obesity-inducing PVH lesions. Measurements of resting insulin levels at the end of the experiment revealed hyperinsulinemia in the VMH and CUT groups but normal insulin values in the PVH group. These results demonstrate that VMH lesions, PVH lesions, and medial knife cuts produce similar hyperphagia syndromes associated with carbohydrate-specific overeating, but that they differentially affect protein selection and resting insulin levels.
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PMID:Macronutrient self-selection in three forms of hypothalamic obesity. 684 76

The effects of bilateral lesions of the ventromedial hypothalamus (VMH) on daily rhythms of the activity of a gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), in the liver and kidney of rats were examined. PEPCK activity in the liver was considerably lowered by VMH lesions, but its rhythm remained similar to that of control liver. In contrast, PEPCK activity in the kidney was markedly elevated by the lesions. From these findings, it is suggested that the VMH is not the site of the master biological clock of the rhythm of PEPCK activity. Although these results do not exclude the possibility that hyperphagia and hyperinsulinemia associated with VMH lesions induce changes in the levels of PEPCK activities, they support the hypothesis that suppression of the sympathetic nervous system causes the changes in PEPCK activity through direct or indirect mechanisms. These findings also suggest that the reciprocal change in PEPCK activities in the liver and kidney after VMH lesions is related to complementary functions of the two organs in maintenance of homeostasis of blood glucose.
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PMID:Reciprocal changes in gluconeogenic enzyme activity in liver and kidney by VMH lesion. 686 26

To improve understanding of the relationships between gastric inhibitory polypeptide (GIP) and insulin secretion and food intake in obesity, immunoreactive insulin and immunoreactive GIP were measured in 5 obese children during PO glucose tolerance test carried out before and after diet. Before diet, mean insulin levels were normal at fasting and rose after glucose ingestion. The mean fasting immunoreactive GIP level was very high (1235 +- 209 pg/ml) compared to that of 8 healthy adult controls (411 +/- 44 pg/ml) and remained at this level throughout the test. There was only a short postabsorptive rise to 1515 +/- 158 pg/ml at 30 min, which was not significantly different either from the patients' basal values or from the 30-min control values (1356 +/- 67 pg/ml). After dieting for 3 to 7 months, immunoreactive insulin responses returned to normal ranges. Concomitantly, both basal and total GIP release diminished significantly (basal GIP, 343 +/- 92 pg/ml; area under the GIP curve, 3820 and 1694 pg/ml/hr before and after diet, respectively). The postabsorptive GIP increment, however, rose significantly from 180 pg/ml/hr, before diet, to 665 pg/ml/hr afterwards. These results might be compatible with the hypothesis that in obesity, hyperinsulinemia, and overactivity of the GIP cells are associated phenomena caused by overeating and reversed by reduced food intake. However, several contradictory findings remain unexplained. The discrepancy between insignificant postabsorptive GIP increments and elevated insulin responses before diet casts doubts on the causal relationship between GIP and insulin secretion. The small GIP rise might be due to a limited secretory capacity of the GIP cells or to a diminished stimulatory capacity of glucose. The constantly high level of GIP might reflect chronic hypersecretion and/or some defect in basal regulation and feedback control of GIP release. The change caused by dietary measures in the GIP secretion pattern provides evidence that in obese children, basal GIP secretion in influenced by nutritional factors.
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PMID:Effects of diet on insulin and gastric inhibitory polypeptide levels in obese children. 699 Mar 66

Diabetes in the C57BL/KsJ(db/db) mouse is initially expressed as hyperinsulinemia, followed by hyperphagia, progressive obesity, and widespread pathologic abnormalities. This study was designed to evaluate the effects of metabolic control on the natural history of the diabetic nephropathy. Beginning at 1 mo of age and continuing for 12 wk, diabetic mice were subjected to controlled dietary restriction, such that their weight was maintained similar to that of age-matched, nondiabetic heterozygotes. Diet-restricted diabetics were compared with diabetics fed ad libitum and heterozygote nondiabetics. Significant lowering of fasting blood glucose, water intake, and plasma insulin was achieved by diet restriction. The diet-restricted diabetes demonstrated enhanced metabolic efficiency, consuming approximately half as much food as the nondiabetics, while maintaining a similar weight. Diabetics fed ad libitum evidenced well-defined renal lesions that included 3 + to 4 + immunoglobulin deposition in the glomerular mesangium, and generalized mesangial matrix expansion. These lesions were completely prevented in diet-restricted diabetes whose glomeruli were normal light microscopy, and demonstrated trace to 1 + mesangial immunoglobulin deposition, features identical in all respects to the nondiabetics. These results indicate that diabetic control achieved by preventing of obesity in the db/db mouse prevents the development of diabetic nephropathy.
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PMID:Prevention of diabetic nephropathy by diet control in the db/db mouse. 700 65


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