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

Rat body size and tissue composition changes from pre-weaning to three months age resulted from voluntary hyperphagia triggered by offering a cafeteria diet. The effects of a 24 hour starvation period in both cafeteria and chow fed controls were compared. Obesity develops earlier in females than in males. This difference is related to the growth patterns in both sexes. Obesity occurs at the stages of development when growth rate decreases. Cafeteria fed female rats attained a 32% greater weight than their controls, with lumbar adipose cords that were 4 times heavier and brown interscapular adipose tissue 2 times heavier than controls. The overall cafeteria fed versus chow fed rat differences in the effects of a 24 hour starvation, were minor but less liver glycogen and much more skeletal muscle lipids were mobilized in the cafeteria fed rats than in controls.
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PMID:Body weight and tissue composition in rats made obese by a cafeteria diet. Effect of 24 hours starvation. 339 32

The body temperatures of mature lean and obese C57BL/6J mice were measured just after feeding, during ad libitum access to food, or every 24 h throughout a 3-day fast. Obese mice had body temperatures 1.0-1.4 degrees C lower than lean mice in the postprandial state and during ad libitum feeding. During food deprivation, obese mice became more hypothermic than lean sex-matched controls. A 5 degrees C fall in body temperature was observed in mutant females in the first 24 h of starvation, about twice that seen in any other experimental group. Over the same period the temperature changes of obese males and lean females were similar and both groups had larger hypothermic responses than lean males. The present results indicate that both genotype and gender affect thermoregulation in these mice. Under normal colony room conditions (ad libitum feeding, 23 degrees C) the ob/ob mutation is expressed by lower body temperatures which along with hypoactivity and hyperphagia account for the high rates of energy storage. When food availability is limited, females of both phenotypes display an increased capacity to reduce their maintenance energy requirements by lowering body temperatures. This hypothermia may be responsible for both the increased conservation of body mass seen during starvation and the slightly greater (5%) fat stores observed in female mice.
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PMID:Fed and fasting thermoregulation in ob/ob mice. 406 46

1. The effects of food intake and the fatty acid composition of the diet on the hepatic stearoyl-CoA desaturase activity of obese-hyperglycaemic (ob/ob) mice were investigated. 2. Obese mice fed on a commercial mouse diet, ad libitum, had 6.5-fold more activity per liver cell than had lean mice. 3. On a diet containing 14% corn oil the activity was 65% less in obese mice and 62% less in lean mice compared with animals fed on the commercial diet. 4. Feeding with 14% saturated fat in the diet doubled the activity in lean mice compared with those on the commercial diet, but had no effect on the activity in obese mice. 5. Obese mice fed on the corn-oil diet contained a higher proportion of linoleic acid in the liver lipids than did lean mice fed on the commercial diet, but the acyl-CoA desaturase activity was 125% higher than in the lean mice. 6. Limiting the food intake of obese mice by pair-feeding with lean mice decreased their acyl-CoA desaturase activity when the animals were fed on the saturated-fat diet, but the activity remained 75% higher than in lean mice, whereas in obese mice pair-fed on the corn-oil diet the activity was the same as in lean mice. 7. During starvation the acyl-CoA desaturase activity in livers from obese mice decreased more slowly and proportionately less than in livers from lean mice. 8. It is concluded that increased substrate supply as a result of hyperphagia and not low concentration of linoleic acid is the main factor causing high acyl-CoA desaturase activity in obese mice.
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PMID:The regulation of hepatic stearoyl-coenzyme A desaturase in obese-hyperglycaemic (ob/ob) mice by food intake and the fatty acid composition of the diet. 612 73

Modulation of feeding by opiates, putative satiety peptides, and dopamine was explored in the Chinese hamster, an animal that develops diabetes mellitus in certain inbred strains. Diabetic hamsters were hyperphagic relative to their nondiabetic controls, but both groups exhibited natural circadian variation in feeding. Starvation provoked hyperphagia of about 1-h duration in both groups. Naloxone and butorphanol had no effects on Chinese hamster feeding. Opiate receptor binding on Chinese hamster brains demonstrated no specific binding of naloxone or ethylketocyclazocine, but IR-dynorphin concentrations were comparable with that in rats. N-allylnormetazocine, a sigma-opiate receptor agonist, appeared to stimulate diabetic hamster feeding. Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. Calcitonin limited feeding in both groups but may be nonspecific. Dopaminergic blockade by haloperidol also limited feeding, and diabetic hamsters were more sensitive to this. Although Chinese hamsters clearly can modulate their food intake when diabetic, we conclude that the opiatergic and peptidergic influences on feeding are very different from those in rats and may be of little importance.
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PMID:Feeding systems in Chinese hamsters. 614 21

The adaptive regulation of sugar and amino acid transport by vertebrate intestine constitutes a neglected area. We review the patterns, signals, and mechanisms involved in adaptation. Mechanisms include changes in mucosal mass, specific transport systems, and the sodium gradient. Signals include the transported solutes themselves, hormones, and pancreaticobiliary secretions. The pattern of adaptation is examined for effects of dietary solutes, starvation, hyperphagia, dietary bulk, diabetes, intestinal position, intestinal resection, time of day, season of the year, hibernation, gestation, lactation, and aging and for differences among species. These observed patterns are compared with the patterns predicted by a simple teleologically deduced hypothesis: increased metabolic requirements should be met by increased absorption achieved through increased mucosal mass, while nutritionally essential solutes and nonessential solutes used as calorie sources should, respectively, repress and induce their own transport. We conclude with a summary of major unsolved questions in this area.
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PMID:Adaptive regulation of sugar and amino acid transport by vertebrate intestine. 635 41

Payne & Dugdale (1977) have proposed a model for predicting body weight in humans when the individual lean : fat tissue deposition ratio, energy intake +/- s.d. and energy expenditure +/- s.d. are known. The model was tested in 8 individuals, whose actual weights, energy intakes and expenditures (with their standard deviations) for a normal period, a semi-starvation period and an overfeeding period of 2 weeks were known or estimated. With the model, the lean : fat tissue deposition ratio for each person was calculated from the data of the semi-starvation period. From this ratio the model was able to predict a body weight equal to the one observed for the normal period. For the overeating period, the model predicted body weights which were considerably higher than the ones observed. Some explanations for this phenomenon are discussed.
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PMID:Prediction of weights in humans after overfeeding using the Payne-Dugdale model. 652 19

Recovery of body weight and food intake have been studied and compared after a 25% weight loss produced by total starvation in one group of rats or by food restriction in a second group. It was shown that rats in both groups returned to their initial body weight within the same time on the average, but the hyperphagia observed during the recovery phase was significantly higher in restricted than in starved rats. In the former, the increase of food intake fully accounted for the weight gain. On the contrary, the recovery of body weight in previously starved rats involved both hyperphagia and a long lasting persistence of the fasting hypometabolism. In addition, it was shown that in those rats the higher the contribution of hypometabolism the longer the recovery. Starvation diabetes was higher in starved than in restricted rats and might be one factor which impairs weight regulation through hyperphagia after a weight loss induced by food deprivation.
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PMID:Recovery of body weight following starvation or food restriction in rats. 692 12

The effects of starvation and refeeding and of obesity on pancreatic alpha2- and beta-cell responses to glucose or tolbutamide were studied with the isolated rat or mouse pancreas perfused with an amino acid mixture in the presence and absence of glucose. It was observed that the physiological adaptation to a regimen of fasting and realimentation and to obesity differed greatly in the two types of endocrine cells. Whereas beta-cells of rats showed a dramatic reduction of glucose- and tolbutamide-stimulated insulin release during starvation that was reversed by refeeding, alpha2-cells preserved their response to stimulators and inhibitors during this experimental manipulation. Amino acid stimulation of glucagon release occurred equally well with the pancreas from fed and starved rats and was suppressed efficiently by glucose and tolbutamide in both nutritional states. Surprisingly, the rate of onset of glucose suppression of alpha2-cells was significantly higher in the fasted than in the fed state. This glucose hypersensitivity was apparent 2 d after after food deprivation and had disappeared again on the 2nd d of refeeding. In the pancreas from animals starved for 3 d, glucose and tolbutamide suppression of alpha2-cells took place in the absence of demonstrable changes of insulin release. In the isolated perfused pancreas taken from the hyperphagic obese hyperglycemic mouse (C57 Black/6J; ob/ob), the observed rate of insulin secretion as a result of a combined stimulus of amino acids and glucose and of glucagon release stimulated by amino acids was about four times higher than achieved by the pancreas of lean controls. However, glucose was unable to suppress the alpha2-cells in the pancreas of obese animals, in spite of the hypersection of the beta-cells, again in contrast to the alpha2-cells of controls that were readily inhibited by glucose. These data imply that the acute suppression of alpha2-cells by glucose is largely independent of a concomitant surge of extracellular insulin levels and that the adaptation of the islet organ to starvation leads to decreased glucose sensitivity of beta-cells, which contrasts with an improved glucose responsiveness of alpha2-cells. However, hyperphagia, which is assumed to be the primary abnormality in the ob/ob mouse, leads to overproduction of insulin and glucagon by the pancreas while greatly reducing the alpha2-cell sensitivity to glucose. An attempt is made to incorporate these data on starvation, refeeding, and obesity, as well as previous results with experimental diabetes, in a comprehensive picture describing a regulative principle underlying the glucose responsivness of alpha2-cells.
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PMID:Adaptations of alpha2- and beta-cells of rat and mouse pancreatic islets to starvation, to refeeding after starvation, and to obesity. 698 16

The effects of sex, castration and estrogen treatment of castrated rats subjected to starvation-refeeding were studied. Food intakes, liver lipid levels and the activities of glucose 6-phosphate dehydrogenase and malic enzyme in ad libitum-fed, starved and starved-refed rats were determined. Sex differences observed in the intact ad libitum-fed rats could be explained in part by the differences in estrogen levels. Sex differences were obliterated in the starved-refed intact rats but were observed when castrated female starved-refed rats were compared to castrated male starved-refed rats. The differences could not be erased with the administration of estrogen. Estrogen significantly reduced food intake of castrated rats. Results of this study suggest that the characteristically higher liver lipid level and enzyme activity in the female, compared to the male, may reflect the female's tendency to undereat when circulating estrogen levels are high and to compensate (by overeating) for this undereating when estrogen levels are low.
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PMID:Effects of estrogen on the responses of male and female rats to starvation-refeeding. 702 78

The individual response to overeating and semistarvation on energy expenditure at rest and light work before and after a test meal was investigated. This response was related to the change in dry body weight, measured as weight (W) minus total body water (TBW). Experiments were performed on 9 non-obese subjects: (a) with a normal habitual energy intake; (b) (overfeeding) with an extra energy intake of 12 MJ per day for two weeks; and (c) (semistarving) with an energy intake of only 2.1 MJ per day for 2 weeks. Measurements of VO2, VCO2, W and TBW were obtained at the end of each of the three periods. It was found that the perturbation in energy intake from normal to 20-25 MJ per day increased the energy expenditure. The magnitude of this increase was highly individual and inversely related to the change in dry body weight. Energy expenditure, measured under the four standardized conditions, after 2 weeks of starvation was lower than that obtained after the preceding overeating period. This decrease was also roughly inversely related to the change in dry body weight. The results support the idea that part of the regulation of body energy content takes place by way of a change in the efficiency of energy utilization and that the response to a perturbed energy intake varies considerably between subjects.
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PMID:Effects of excessive caloric intake and caloric restriction on body weight and energy expenditure at rest and light exercise. 713 41


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