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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immature male rats were overfed for a long time with an excess of fats or carbohydrates; this caused obesity. Carbohydrate overfeeding led to a greater body weight gain and a greater increase in the weight of epididymal fat and of the adipose cell volume than fat overfeeding, but failed to decrease the lipolytic activity of the aorta. Prolonged fat overfeeding decreased the lipolytic activity of the aorta considerably. Thus, the results of the mentioned experiments showed that the predisposition of the aortic wall to atherogenesis did not correlate with the gain in weight and depended on the character of nutrition.
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PMID:[Effect of different types of excessive feeding on the state of vascular walls in rats]. 101 2

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

The fat cells of rat epididymal adipose tissue contain an average of 0.5 mg of cholesterol per gram of triglyceride. Of this cholesterol, 90% is nonesterified and 80% is located in the lipid storage compartment. The fat cell cholesterol content correlated positively with cell size. During fasting the free cholesterol of the adipocyte decreased in parallel with triglyceride, whereas the amount of esterified cholesterol did not change. The fat cell cholesterol content is independent of the amount of dietary cholesterol. On in vitro incubation of rat fat cells with radiolabeled acetate, mevalonate, glucose, leucine, or water, labeled cholesterol was synthesized. The rate of cholesterol synthesis increased with fat cell size. Fasting suppressed cholesterol synthesis by 90%, whereas refeeding stimulated the synthesis above values found in normally fed rats. Stimulation of lipolysis with theophylline or with dibutyryl cyclic AMP markedly inhibited cholesterol synthesis in fat cells. Insulin increased the incorporation of glucose and leucine into fat cell cholesterol. The cholesterol synthesis in fat cells was not suppressed by a high cholesterol diet. Addition of very low or low density lipoprotein into the incubation medium suppressed fat cell cholesterol synthesis whereas high density lipoprotein did not. The lipoprotein-free serum stimulated cholesterol synthesis compared with serum-free medium. The rate of cholesterol synthesis in total adipose tissue of rat was estimated to be 4% of that in the liver. It seems unlikely that the increased body cholesterol turnover present in obesity is accounted for by the enhanced cholesterol formation in the enlarged adipose tissue.
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PMID:Regulation of cholesterol synthesis and storage in fat cells. 112 58

Experiments were carried out to elucidate the mechanism of triglyceride accumulation in epidiymal adipose tissue of obese mice made by goldthioglucose injection. Specifically, fat mobilization and its deposition were investigated. In goldthioglucose-treated mice, the weight of the epididymal adipose tissue was 1,200 percent of that of control mice, while adrenaline-induced lipolysis and lipase activity of the tissue were 272 and 450 percent of control respectively. These results suggest that deposition of fat far exceeds fat mobilizing activity in the adipose tissue of the obese mice. It was found that triglyceride synthesis from glucose increased in the adipose tissue of these mice. Therefore, it is suggested that obesity in gold thioglucose-treated mice may not be due to decrease in fat mobilization but to increase in triglyceride synthesis from carbohydrate.
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PMID:Triglyceride metabolism in epididymal adipose tissue of obese animals. 122 94

Recent studies have found that angiotensinogen is expressed in white and brown fat pads, and adipocytes have been implicated as a primary source of angiotensinogen in several other tissues. The functional significance of this unexpected expression is unknown. To address this, we studied angiotensinogen messenger RNA (mRNA) expression and angiotensinogen secretion in adipose tissue and isolated adipocytes comparing fasted and refed rodents and those with genetic obesity with normal controls. Control 2-month-old Sprague-Dawley rats, those fasted for 3 days, or those fasted for 2 days and refed for 6 days were killed, and adipocytes were isolated from epididymal fat pads using collagenase digestion. Angiotensinogen mRNA was reduced to 14.6 +/- 2.3% of control levels under fasted conditions and increased to 228 +/- 53% of control levels after refeeding. Angiotensinogen release from adipocytes was reduced to 33% of control levels by fasting and increased to 183% by refeeding. These effects of fasting and refeeding on angiotensinogen regulation were tissue specific since liver angiotensinogen mRNA and serum angiotensinogen concentrations were unaffected. Systolic blood pressure, however, was modulated by fasting and refeeding in a manner parallel to adipocyte angiotensinogen expression. In related experiments, angiotensinogen secretion per epididymal fat pad of the ob/ob mouse model of obesity was increased an average of 3.4-fold compared with control. We conclude angiotensinogen expression in white adipocytes is regulated nutritionally in a tissue-specific manner. We propose that adipocyte angiotensinogen could play a previously unrecognized role in regulating adipose tissue blood supply and thereby fatty acid efflux from fat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue-specific nutritional regulation of angiotensinogen in adipose tissue. 155 65

1. Groups of lean and obese male SHR/N-cp rats were fed isoenergetic diets containing 54% carbohydrate as cornstarch (CS) or sucrose (SU) plus other nutrients from 5 weeks of age, and measures of adiposity, thyroxine 5' deiodinase (T4-5'DI) activity, and tissue and plasma triiodothyronine (T3) content determined at 9.5 months of age. 2. Body weights (BW) of obese greater than lean, and were greater when fed the SU than CS diet in both phenotypes. Phenotype effects (obese greater than lean) were present for fat pad weights and adipose cellularity in most primary adipose tissue depots, and diet effects (SU greater than CS) were present for epididymal and retroperitoneal depots in both phenotypes. 3. Interscapular brown adipose tissue (IBAT) and IBAT:BW ratios of obese greater than lean, and diet effects (SU greater than CS) were present for lean but not obese rats. Liver T4-5'DI activity and plasma and tissue T3 of lean greater than obese, while IBAT 5'DI activity of obese greater than lean in the CS diet. 4. These results indicate that obesity occurs in the SHR/N-cp rat as the result of hypertrophy and hyperplasia of adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate exaggerates fat accretion in lean but not obese rats. Moreover, the obesity occurs in spite of greater mass, cellularity, and T4-5'DI activity of IBAT, consistent with a thermogenic defect in the obese phenotype of this strain.
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PMID:Effects of diet and phenotype on adipose cellularity and 5'-deiodinase activity of liver and brown adipose tissue of diabetic SHR/N-cp rats. 167 39

Lean and obese Zucker fatty rats were adrenalectomized or sham operated at 10 wk of age. At 15 wk one-half of each group was placed on a high-fat diet. At 32 wk of age the experiment was ended. Several conclusions can be drawn about the effects of adrenalectomy, high-fat diets, and their interaction in the Zucker fatty rat. First, adrenalectomy slowed the weight gain in both obese fatty rats and in the lean animals, although the effect was greater in the fatty rats. Second, weight gain was accelerated in intact lean and fatty rats eating a high-fat diet. Third, adrenalectomy attenuated the weight gain associated with a high-fat diet and reduced the body content of fat and protein in the lean animals and fatty rats fed the low-fat diet. Fifth, adrenalectomy significantly affected the retroperitoneal and subcutaneous fat depots but not the epididymal fat depot. Sixth, adrenalectomy decreased fat cell number in retroperitoneal and subcutaneous fat depots, but this was much less evident in the epididymal fat depot. Seventh, lipoprotein lipase activity expressed per milligram protein increased after adrenalectomy in the fatty rat but was reduced on the same basis in lean animals regardless of diet. Finally, the increase in retroperitoneal lipoprotein lipase activity expressed per fat cell observed in lean animals fed the high-fat diet was not observed in the fatty rat. These studies show that a high-fat diet and adrenalectomy interact in the development of obesity in both lean and fatty Zucker rats.
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PMID:Effect of adrenalectomy and high-fat diet on the fatty Zucker rat. 173 48

Effect of hypothalamic lesions on regulation of body weight and fat cell dynamics in obese mice were examined during refeeding after prolonged food deprivation. Obese mice, which were treated with monosodium glutamate for 5 postnatal days and had ventromedial nuclear lesions in the hypothalamus, were used. When adult obese mice were given a glucose electrolyte solution for 20-40 days, the body weight dropped to about 45% of their pre-treatment weight. After reinstituted feeding of normal mouse food ad libitum, their body weight and adipose tissue weight returned to pre-starvation level. Tritiated thymidine autoradiography revealed that cell proliferation occurred in the early stages of refeeding and some fat cells were renewed in the epididymal adipose tissue. Fat cell renewal was found more active in the experimental group than in the control. Thereafter, fat cell size increased gradually via fat storage. These obese mice were found to have the capacity to regulate their body weight and adipose tissue not only through fat storage but also by increasing number of fat cells, in order to replace the cells which were lost during starvation. Therefore, ventromedial nuclear lesion in the hypothalamus does not influence the regulatory mechanism of adipose tissue during starvation and refeeding.
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PMID:Adipocyte dynamics in hypothalamic obese mice during food deprivation and refeeding. 180 74

With the identification of two different glucose transporter species in adipose cells it is crucial to determine the role of these transporters in the alterations in glucose transport activity associated with different metabolic and nutritional states. In the present study we assess levels of expression of Glut 1 and Glut 4 transporters and basal and insulin-stimulated glucose transport activity in adipocytes from Sprague-Dawley rats fed standard chow (control), combined liquid diet and standard chow (overfed), high fat diet, or energy-restricted diet for 7 weeks. High fat feeding was associated with relative postprandial hypoglycemia (P less than 0.05) and hypoinsulinemia (P less than 0.05). Although the high fat fed animals had lower body weights (P less than 0.05) than control rats, their body compositions showed obesity, with 36% heavier epididymal fat pads (P less than 0.05) and a 47% increase in adipocyte volume (P less than 0.05). Fat feeding caused a 78% reduction in insulin-stimulated glucose transport per adipocyte (P less than 0.05). In parallel we found 92% and 94% reductions in Glut 4 protein and mRNA per adipocyte, respectively, (P less than 0.01) in fat-fed rats. Substantial reductions were also seen in Glut 1 protein and mRNA per fat cell in the same rats (62% and 76%, respectively; P less than 0.05). However, the changes in Glut 1 expression were of the same magnitude as changes in the cytoskeletal protein beta-actin, reflecting a decreased expression of several proteins in this nutritional state. Even though overfeeding and energy restriction brought about opposite changes in adiposity, no significant alterations were demonstrated in glucose transport rate or glucose transporter expression. The impaired insulin-stimulated glucose transport in adipose cells from high fat-fed rats occurs in the presence of a dramatic decrease in the expression of the major insulin-responsive glucose transporter (Glut 4). The reduced gene expression may be caused by chronic hypoinsulinemia and may contribute to the insulin resistance observed in this state.
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PMID:High fat feeding causes insulin resistance and a marked decrease in the expression of glucose transporters (Glut 4) in fat cells of rats. 185 75

The short-term effects of adrenalectomy on certain aspects of glucose homeostasis and adiposity were examined in Zucker and Wistar diabetic fatty (WDF) rats. Ten-week-old male obese and lean WDF and Zucker rats were adrenalectomized or underwent sham operation. Obese rats of each strain were pair fed the intake of obese adrenalectomized rats. Intragastric glucose tolerance tests showed that sham-operated obese rats of both strains were severely hyperinsulinemic compared with leans; adrenalectomy and pair feeding reduced palsma insulin to lean levels in Zucker but not WDF rats. At the time they were killed, sham-operated obese WDF rats were significantly hyperglycemic and hyperinsulinemic compared with other groups, but adrenalectomy reduced plasma glucose and insulin to lean levels in both strains. Adrenalectomy reduced inguinal and retroperitoneal fat pad weights more in Zucker than WDF obese rats. Although adrenalectomy decreased epididymal and inguinal fat cell size in both obese rat strains, the effect was greater in Zucker compared with WDF rats. These data suggest that the basis for the differential response to adrenalectomy in obese WDF and Zucker rats may reside in their different genetic backgrounds.
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PMID:Zucker and Wistar diabetic fatty rats show different response to adrenalectomy. 192 36


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