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

A new strain of obese mouse, the PBB/Ld, has been studied in terms of fat pad cellularity, serum insulin and blood glucose levels, and response to gold thioglucose injections. Age-matched C57B1/6J mice were used as controls. Adipocyte size and number in the major fat depots were determined at various ages from weanling to maturity in the PBB/Ld and C57B1/6J strains. Results indicated that obesity in the PBB/Ld was due to hypertrophy of adipocytes in retroperitoneal and subcutaneous fat depots and to hypertrophy and hyperplasia in the epididymal fat pad. PBB/Ld mice also developed hyperinsulinemia and hyperglycemia and these findings have been discussed in terms of the developmental changes in fat pad cellularity. The injection of gold thioglucose led to increased food intake in both PBB/Ld and C57B1/6J mice. Hyperphagia was also present in the PBB/LD control group, but increased efficiency of converting calories to body weight was not observed in this group when compared to control C57B1/6J mice. The characteristics of obesity seen in the PBB/Ld mouse are discussed and comparisons are made to similar studies in other rodent models of obesity.
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PMID:Description of obesity in the PBB/Ld mouse. 34 7

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

1. Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured. 2. Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7, and 8 d of age; 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about 120% in both sexes at 20-30 weeks old. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-eright of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values. 3. Obesity was not detected in the offspring of female mice that had received 100 g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning. 4. Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected. 5. The addition of 20 g MSG/l to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice. 6. The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age. 7. The obesity induced in mice by MSG was not associated with hyperphagia, unlike genetic obesity and obesity induced by gold thioglucose (GTG). 8. All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content. 9. Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50-120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost 100% reliable in inducing a high extent of adiposity.
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PMID:The induction of obesity in rodents by means of monosodium glutamate. 110 64

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning mice were fed ad lib. At 13 weeks of age some mice from large litters received gold thioglucose (GTG: 600 mg/kg intraperitoneally) to induce hyperphagia, and mice were killed at 13, 19.5, 26, 39 and 52 weeks. 2. Total carcass lipid and the size and number of adipocytes in the inguinal subcutaneous, genital, perirenal and mesenteric depots were determined. 3. Mice, both male and female, raised in small litters were heavier and had more carcass fat at all ages than mice raised in large litters. After GTG-treatment mice from large litters were heavier and fatter than mice raised in small litters. 4. Fat distribution between the depots was related to carcass lipid content and not to treatment. The order of depot development was subcutaneous, parametrial, perirenal and mesenteric in females and epididymal, subcutaneous, perirenal and mesenteric in males. At 13 weeks the depots in males were more developed than those in females. 5. Litter size had no effect on adipocyte volume in female mice at 13 weeks but by 52 weeks small-litter mice had larger cells in all depots and more cells in the parametrial and perirenal depots. 6. Male mice from small litters had bigger cells at 13 weeks in all depots compared with males from large litters but by 52 weeks no significant differences remained. Greater numbers of cells were present only in the perirenal and mesenteric depots of small-litter males at some ages. 7. Depots of GTG-treated large-litter female mice had larger cells than those of small-litter females, while a similar number of cells was found by 52 weeks in all but the perirenal depot, which had significantly more cells. 8. GTG treatment of male mice from large litters also caused bigger cells than in small-litter mice, and an increased depot cell number at earlier ages in all but the epididymal depot. By 52 weeks cell numbers were similar in depots from small-litter and GTG-treated large-litter mice, except for the epididymal depot from the latter which had fewer cells. 9. Increases in cell numbers with age in different depots occurred independently of existing cell mean volume and even of tissue growth, suggesting the presence of an in-built chronology, at least in older mice.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study. 313 38

In order to test whether or not overeating of a nutritionally adequate diet with reasonable fat content could result in significant fat accumulation in the liver, male Sprague-Dawley rats were provided with free access to either a nutritionally adequate liquid diet with 35 per cent of calories as fat or a regular diet (controls) for 3 months. After the feeding period, body weight, Lee index, and epididymal adipose tissue weight, were significantly greater in rats fed with the liquid diet than in the controls. Liver weight, hepatic triglyceride levels were also greater in the liquid diet group. Histologically, remarkable fatty infiltration was observed predominantly in periportal areas in rats fed with the liquid diet ad libitum for 3 months. Compared to a large body of the literature concerning diet-induced obesity in experimental animals, information on animal models of fatty liver by dietary manipulations is insufficient. The results of this study clearly indicate that the overeating of a nutritionally adequate diet with reasonable fat content could result in remarkable fat accumulation in the liver in rats.
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PMID:Fatty liver in rats induced by excessive intake of a nutritionally adequate liquid diet. 344 Jun 81

The insulin-degrading activity of liver supernatants and epididymal adipose-tissue homogenates from genetically obese-hyperglycaemic mice (ob ob) and their lean litter mates was studied by measurement of radioactive trichloroacetic acid-soluble degradation products of the insulin molecule. Optimum assay conditions for the decomposition of the hormone were devised. The properties of the degrading activity suggested the presence of enzymic insulin destruction in both the liver and epididymal adipose tissue. There was no difference in insulin degradation in liver samples from obese and lean mice when the results were related to the protein content of the supernatants. The epididymal adipose-tissue homogenates from obese mice displayed about eightfold higher degrading activity per unit of protein than did homogenates from lean animals. The physiological significance of this finding is discussed in the light of the increased fat depots, hyperphagia, raised serum insulin concentrations and increased insulin tolerance previously recorded in this strain of mice.
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PMID:Degradation of insulin in vitro by liver and epididymal adipose tissue from obese-hyperglycaemic mice. 563 59

BAY g 5421 (acarbose) inhibits carbohydrate digestion in the gut, thereby reducing the rate of glucose absorption. This experiment tested whether long term administration of acarbose to developing Zucker "fatty" (fafa) rats would, by reducing several lipogenic factors, attenuate lipid deposition and reduce the hyperphagia and increased food motivated behavior of these animals. From 7 to 20 weeks of life groups of fatty and lean (FaFa) control rats were fed 0, 20 or 40 mg acarbose/100 g maintenance diet (45% carbohydrate, 35% fat, 20% protein calories), while an additional fatty and lean group were pair-fed to respective 40 mg acarbose groups. Lean groups fed acarbose exhibited dose dependent reductions of body weight, insulin, triglycerides, retroperitoneal and epididymal pad weight, adipocyte size, LPL activity/cell (retroperitoneal pad only), and lipid deposition both in total grams of fat and as a percentage of carcass weight. Fatty groups fed acarbose exhibited dose dependent reductions of insulin, blood glucose, retroperitoneal pad weight, and, at one of the two doses used, significantly lowered body weight, (40 mg), triglycerides (20 mg) and cholesterol (20 mg). However, acarbose-fed fatty groups failed to show significant reductions of adipocyte size, number or LPL activity/cell in retroperitoneal and epididymal fat pads, and maintained their obese body composition, on a percentage basis, at levels not significantly different from that of the 0 mg fatty control group. Acarbose administration led to an initial dose dependent reduction of food intake in both genotypes, which persisted for the lean groups. Fatties fed the 20 mg dose showed a gradual tendency (ns) towards increased daily intake, lever pressed at elevated rates for food pellets, and refed at faster rates following fasting. Fatties fed the 40 mg dose maintained their daily intake at fatty control levels, did not lever press at elevated rates, and showed significantly reduced refeeding following fasting. The 40 mg fatty and both lean acarbose treated groups had decreased sucrose solution preference. Possible bases for these differing effects of the drug on feeding behavior by the groups are considered.
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PMID:Effects of a glucosidase inhibitor (acarbose, BAY g 5421) on the development of obesity and food motivated behavior in Zucker (fafa) rats. 662 10

Obese-hyperglycemic mice show hyperphagia and hypothyroidism. The reduced body temperature can be normalized by injection of thyroxin. Limiting food intake to normal non-obese levels reduces blood sugar level, insulin content of the blood and body weight. However, reduction of all these parameters together until normal level occurs only when combining thyroxin injection with restricted diet. Weight of epididymal fat pad, nuclear volume of Leydig cells and volumes of islets of Langerhans normalize too during the combined treatment. It is argued that in adult obese mice hyperphagia and hypothyroidism are two separate factors which cannot be completely compensated for one by another. At least some symptoms in the obese-hyperglycemic syndrome could be attributed to hypothalamic disturbances caused by a reduced thyroidal activity at a very early age after birth.
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PMID:The role of hyperphagia and hypothyroidism in the development of the obese-hyperglycemic syndrome in mice (ob/ob). 694 82

Polygenic obese (M16) and nonobese (ICR) mice were fed ad libitum either a high-fat (FAT) or high-carbohydrate (CHO) diet from 6 to 10 weeks of age. After this four-week period, M16 exceeded (P less than 0.01) ICR mice and FAT-fed exceeded (P less than 0.01) CHO-fed mice in body energy percent, body fat percent, and weight and proportional weight of epididymal and subcutaneous fat pads. Fat cell size and number in both fat depots were greater (P less than 0.01) in the M16 than in the ICR line. Mice fed FAT had larger (P less than 0.01) fat cells in both depots compared with CHO-fed mice, but fat cell nuber was not altered significantly. M16 mice were hyperglycemic, hyperinsulinemic and hypercholesterolemic, Dietary treatment did not affect glucose or insulin levels, but cholesterol was greater (P less than 0.01) on FAT than on CHO diet. Lipoprotein lipase and fatty acid synthetase activities were greater in M16 than in ICR mice, while fatty acid synthetase activity was greater in mice fed CHO than in those fed FAT. Genotype by diet interactions were not important for the traits studied. Polygenic obese mice, developed by selection for increased growth rate, share many of the characteristics of the single gene obesity syndromes in rodents. The development of obesity in polygenic obese mice may be due, in part, to an acceleration of the normal developmental process of growth, in addition to hyperphagia and increased energetic efficiency.
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PMID:Adipose cellularity, serum glucose, insulin and cholesterol in polygenic obese mice fed high-fat or high-carbohydrate diets. 703 Aug 75

Acute central administration of galanin has been reported to increase fat consumption. These experiments were designed to test the hypothesis that repeated injections of galanin would elicit hyperphagia and weight gain and that this response would depend on the available diet. Male Sprague-Dawley rats were fed high (56% energy) or low (10% energy) fat diets. Galanin (300 pmol) or saline vehicle was injected into the third ventricle twice daily for 7 days and three times daily for another 6 days. On both the high-carbohydrate and high-fat diets, twice daily galanin increased daytime food intake, but there was a compensatory decrease in nighttime intake. The addition of a third, nighttime injection of galanin was ineffective in producing an increase in total 24-h intake. There was no significant increase in body weight during galanin treatment in rats eating either diet although animals eating the high-fat diet gained more weight as reflected by a significant increase in epididymal fat pad weight. Galanin treatment had no effects on serum insulin, glucose or corticosterone concentrations, measured at the end of the experiment. However, animals fed the high-fat diet had significantly higher insulin concentrations at the time of sacrifice. Although repeated central infusions of galanin reliably stimulated daytime intake of both diets, they failed to increase total daily energy intake or body weight.
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PMID:Chronic cerebroventricular galanin does not induce sustained hyperphagia or obesity. 753 42


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