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

The catabolic effect of bilateral lesions in the ventromedial are of the hypothalamus (VMH) was studied in nitrogen-balance experiments and compared with the effect of a sham-operation in control animals. A transitory (24 h) increase in urine nitrogen was found in the controls, while in the lesioned animals, a persistent increase was found as long as the animals were fed. Fasting (48 h) eliminated the difference in urea excretion between the groups. Food-dependent effects of the VMH lesion are suggested. The changes in body and organ composition of VMH-lesioned animals, kept for 4 months on a food intake close to normal, were studied. The massive increase of body lipids and marked decrease of body protein and water was primarily due to increased subcutaneous-and abdominal-fat, and reduced skeletal and skin protein. An almost normal composition of the liver and close to normal amounts of protein in the viscera demonstrate that at least some tissues in VMH animals are able to maintain a normal protein content. Hyperphagia as a means to counteract the increased amino acid catabolism and to sustain the lean body mass is discussed.
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PMID:Protein depletion and energy retention in rats with ventromedial hypothalamic lesions. 61 11

Colchicine, a drug which produces a reversible inhibition of intraaxonal transport and synaptic transmission, was used as a reversible neural blocker to investigate the role of the ventromedial hypothalamus (VMH) in the control of ingestive behavior and body weight regulation. Male Sprague-Dawley rats received intracranial microinjections of colchicine into the VMH. Volume and concentration of the colchicine solution were varied to assess specificity of action and dose-response relationship. When colchicine (2 and 4 microgram) was microinjected bilaterally into the VMH, there was a dose-dependent increase in food and water intakes and body weight gain which lasted several days. The acute period of hyperphagia was followed by a marked depression in feeding which persisted until body weight was lowered to control levels. This suppression of feeding appeared to be a consequence of the preceding period of hyperphagia and obesity, since colchicine-treated rats which were pair-fed with controls to prevent obesity continued to maintain normal food intake and body weight gain when later fed ad libitum. The results of this study confirm the importance of the VMH in the long term regulation of feeding, and indicate that reversible neuronal blocking with colchicine is a useful technique for investigating the neural substrates of feeding and other behaviors.
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PMID:Reversible hyperphagia and obesity following intracerebral microinjections of colchicine into the ventromedial hypothalamus of the rat. 67 51

The M16 line of mice, selected for rapid postweaning gain, exhibits polygenically controlled obesity and hyperphagia. The effect of limiting postweaning energy intake on the subsequent growth and development of obesity in M16 mice was investigated. Male mice from M16 and an unselected line (ICR) were provided either ad libitum or limited (congruent to 70% of ad libitum) feed during the rapid postweaning growth period from 4 to 6 weeks of age. Body weights (g) at 6 weeks of age were: ad libitum ICR (31.0 +/- 0.6), restricted ICR (23.8 +/- 0.7), ad libitum M16 (45.0 +/- 0.6) and restricted M16 (30.1 +/- 0.6). In both lines, restricted feed intake severely depressed body fat, lean, ash, and water at 6 weeks. In addition, percent triacylglycerol, fat cell size and number in the epididymal fat pads were lower. Restricted M16 and ICR mice showed a marked compensatory gain in all body components when subsequently fed ad libitum for 10 weeks. All measurements of adiposity at 16 weeks were similar for the restricted and ad libitum regimens within each line. The relative amounts of energy deposited as fat and lean between 4 and 16 weeks were not influenced by restricted feeding, but M16 mice deposited a larger proportion of energy as fat than as lean when compared with ICR mice. The results suggest that fat cell number is determined at a relatively early age in mice and is primarily under genetic control.
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PMID:Effect of postweaning feed restriction on adipose cellularity and body compositon in polygenic obese mice. 70 8

The effects on food intake and body weight in lean and obese Zucker rats were evaluated following substitution in the diet with either 1) poorly absorbable lipid (hydrogenated soybean oil) for corn oil, or 2) nonabsorbable carbohydrate (fiber) for glucose. Lean Zucker rats compensated for the reduced caloric availability of the high-fiber and hydrogenated oil diets by increasing food consumption. In contrast, obese rats did not respond significantly to these dietary alterations and failed to attain caloric balance during the 16-day study. These differences in caloric compensatory responses were reflected in body weight gains. There were no differences in the amount of weight gained by lean rats fed either the high-or low-fiber diets because of compensatory hyperphagia in the high-fiber group. Lean rats fed the hydrogented oil diets gained less weight than controls fed corn oil diets, even in the presence of compensatory hyperphagia, because of the enhanced fecal excretion of water and metabolites caused by the poorly absorbed fat diet. As a result of a delayed and incomplete response to reduced caloric availability, obese rats fed the high-fiber and hydrogenated oil diets gained significantly less weight than the obese rats fed low-fiber and corn oil diets.
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PMID:Caloric compensatory responses to diets containing either nonabsorbable carbohydrate or lipid by obese and lean Zucker rats. 70 86

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

Hepatic fatty infiltration complicating jejunoileal bypass can be massive and may require restoration of gastrointestinal continuity. This fatty infiltration appears to be caused by protein depletion associated with adequate or high carbohydrate intake. The present study has shown that calorie-free amino acid alimentation can reverse these changes. In three of thirteen patients who underwent 12 inch to 6 inch jejunoileal bypass procedures, symptomatic hepatomegaly developed with near total replacement of hepatocytes by massive fatty infiltration. After undergoing liver scan, liver biopsy, and liver function tests, the patients were started on a peripheral infusion of 2L per day of a 4.25 per cent crystalline amino acid solution, allowing for fat mobilization while preserving body protein stores. All oral intake was withheld except for water. At the end of a fourteen to twenty-one day infusion period, serum albumin levels increased by 1 gm in all patients. Decreases in liver volume of 83, 45, and 40 per cent occurred. During the infusion period ketonuria was 4 plus in all patients indicating active lipolysis. Weight loss was impressive (17, 19, and 40 pounds). All patients showed marked symptomatic improvement, and postinfusion liver biopsy specimens showed a return to near normal architecture. Maintenance of normal liver size by a high-protein, low-carbohydrate diet was observed in a five to seven month follow-up period. In contrast to previous studies using standard hyperalimentation solutions, the use of calorie-free amino acid solutions reverses the hepatic fatty infiltration seen after intestinal bypass by mobilization of fat. This fat mobilization does not occur as readily in the presence of large amounts of glucose.
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PMID:Reversal of severe fatty hepatic infiltration after intestinal bypass for morbid obesity by calorie-free amino acid infusion. 80 74

The efficacy of intravenous hyperalimentation in the critically ill patient was evaluated by body composition measurements performed with a multiple isotope dilution technic. The size of the body cell mass was evaluated by measuring the total exchangeable potassium and the intracellular water volume. The total exchangeable sodium and the extracellular water volume were both measured to evaluate the extracellular supporting component of body composition. These measurements were performed in two groups of severely ill patients who were in a chronic catabolic state. The first group of sixteen patients received intravenous hyperalimentation and the second group of eighteen patients served as controls in that they were not hyperalimented. Similar measurements were performed in sixteen normal volunteers to define the normal range for the various body composition parameters. In the nonalimented patients, there was a significant decrease in the body cell mass accompanied by an expansion of the extracellular supporting component of body composition. Similar changes occurred in the patients receiving intravenous hyperalimentation. However, the magnitude of these changes was not great. Thus, intravenous hyperalimentation tended to preserve the body cell mass and prevent expansion of the extracellular component of body composition.
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PMID:Effect of parenteral nutrition on body composition in the critically ill patient. 81 25

In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.
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PMID:Feeding behavior in monkeys with and without lesions of the hypothalamus. 81 9

The effect of a deficiency of calories and/or nitrogen on protein metabolism in the rat was investigated. During the 5 days of the study, the rats received all nutrients except water via intravenous hyperalimentation. Four diets were used: I) 1.25 g amino acids, 12.5 g glucose/day; II) 1.25 g amino acids/day; III) 1.25 g glucose/day; and IV) 12.5 glucose/day. The rate of protein synthesis in heart, lung, muscle, kidney, and liver was estimated by a modification of the technique of Garlick et al. (The diurnal response of muscles and liver protein synthesis in vivo in meal-fed rats. Biochem. J. 136: 935-945, 1973) except that [15N]glycine was used as the tracer. Heart and lung protein synthesis was depressed by both caloric and nitrogen restriction. Muscle protein synthesis was only significantly affected by omission of calories from the diet. Kidney nitrogen content increased with the amino acid diets and decreased with the nitrogen-deficient diets. The major response of the liver to a dietary deficiency was to lose nitrogen via an increase in the rate of liver protein catabolism.
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PMID:Effect of nitrogen and calorie restriction on protein synthesis in the rat. 81 8


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