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

Changes of the pyruvate dehydrogenase complex in liver and epididymal fat pad were examined longitudinally in obese mice (C57BL/6J-ob/ob) and their lean controls as a function of age. Total pyruvate dehydrogenase in liver was expressed on several reference bases because of differences in hepatic cellularity and protein content between obese mice and their age-matched lean controls. When total hepatic pyruvate dehydrogenase was expressed on a protein basis, the enzyme activity was elevated in obese mice older than 28 weeks in age when compared to lean controls of a similar age. However, when expressed on a DNA basis, total pyruvate dehydrogenase activity in livers of obese mice up to 10 weeks in age was increased when compared to the age-matched lean control. The proportion of hepatic pyruvate dehydrogenase in the active form was also augmented significantly in obese mice from 5 to 28 weeks of age. In 18-week-old obese mice, the proportion of total pyruvate dehydrogenase in the active form of adipose tissue was significantly higher than that of the lean controls. When expressed on a DNA basis, total pyruvate dehydrogenase in the fat pad was also increased in obese mice up to 10 weeks in age when compared to age-matched controls. Total pyruvate dehydrogenase activity in the epididymal fat pad was higher in obese mice than the lean controls in animals as old as 32 weeks in age when the enzyme activity was expressed per 100 g body weight. The increase in the active form and total activity of pyruvate dehydrogenase in both liver and epididymal fat pad during the dynamic early phase of obesity would augment the capacity for acetyl-coenzyme A formation necessary in the support of an accelerated lipogenesis and fat deposition.
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PMID:Age-related changes in liver and adipose tissue pyruvate dehydrogenase of genetically obese mice. 671 96

Certain aspects of intermediary metabolism of white (epididymal) and brown (interscapular) adipose tissue (BAT) were studied in cold-acclimated weanling rats with hypothalamic obesity. Groups of rats with ventromedial hypothalamic lesions (VMNL rats) and controls were maintained for four weeks at 6 degrees C and 22 degrees C, respectively. Sham-operated rats served as controls. Cold-acclimated VMNL rats showed greater percent BAT but normal percent epididymal fat pad weight, hypophagia, reduced body weight and body weight gains, hyperdipsia, hyperinsulinemia, normoglycemia and normal circulating fatty acid levels, higher carcass lipid and lower carcass protein. They also exhibited a higher rate of epididymal fat pad lipolysis than the controls, but the increment during cold adaptation was less in the VMNL rats compared with the 22 degrees C-maintained VMNL animals. In-vitro metabolism was determined in both the basal and the epinephrine-stimulated state. Basal-state 14C-palmitate oxidation, BAT fatty acid and lipid contents were increased in VMNL rats but protein content, incorporation into phospholipid and triglycerides, BAT lipolysis and glycolysis were normal in cold-acclimated VMNL rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats, but the epinephrine-stimulated increase in lipolysis only in the cold-acclimated VMNL rats. Whereas at 22 degrees C BAT of VMNL rats showed decreased palmitate oxidation and no change of incorporation into phospholipid and triglyceride, during cold acclimation VMNL rats showed normal BAT metabolism and normal response to epinephrine, except for an increase in lipolysis. The data are in agreement with the observation that hypothalamic-obese mature rats have normal cold survival potential and allow us to extend this fact to the normophagic-obese-weanling rat.
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PMID:Brown adipose tissue metabolism in cold-acclimated weanling rats with hypothalamic obesity. 688 32

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

Obese-hyperglycemic mice (genotype ob/ob) have hyperglycemia, hyperinsulinemia, increased resistance to insulin action and decreased insulin receptors on their liver, fat cell and muscle plasma membranes. Hypoglycemic sulfonylureas are reported to improve diabetic control by decreasing the insulin resistance of subjects with Type II diabetes mellitus: however, it is not clear if their mechanism is to increase plasma membrane insulin receptors or to decrease post-receptor insulin resistance. In this study we treated obese-hyperglycemic mice and their normal weight litter mates with the oral hypoglycemic sulfonylurea tolbutamide for 28 to 34 weeks. Tolbutamide administration to normal mice resulted in the following changes that were indicative of increased insulin action: (1) increased body weight; (2) increased epididymal fat-pad weight; (3) increased 2-deoxyglucose transport into the intact diaphragm muscle preparation. There was no alteration in plasma glucose, plasma insulin or pancreatic insulin content suggesting that the tolbutamide effect was an extrapancreatic effect that was probably not mediated by increased insulin secretion. There was no change in the insulin receptor number or affinity of liver cell membranes prepared from tolbutamide treated mice supporting the notion that the extrapancreatic effect of tolbutamide may occur at a post-insulin receptor location. In contrast to the normal mice, tolbutamide did not increase the body weight, epididymal fat pad weight, the already increased 2-deoxyglucose transport into diaphragm muscle or the decreased number of insulin receptors on hepatic plasma membranes. The tolbutamide caused a striking decrease in pancreatic insulin concentration and degranulation of the islets in obese but not normal mice. This is compatible with previous information that the obese mice have abnormal islets that are not under the normal feed-back control of ambient insulin concentration as are the islets of normal mice. We conclude that tolbutamide potentiates insulin action in normal, but not obese, mice and that this potentiation may be due to a post-insulin receptor action.
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PMID:Effect of chronic tolbutamide administration on normal and obese-hyperglycemic mice: evidence for post-receptor potentiation of insulin action. 704 79

Obese and lean alloxan-diabetic rats were given daily injections of insulin for 9 days. Plasma glucose and insulin concentrations were not different between the two genotypes given comparable amounts of insulin. Carcass fat and epididymal and retroperitoneal fat pad weights increased as the dose of insulin was increased. At each of four doses, fatties had larger fat cells, bigger pads, and more body fat than lean rats. Adipose lipoprotein lipase (LPL) activity per pad or per fat cell was increased by insulin. Except for the lowest dose of insulin, LPL activity was higher in obese rats than in lean rats. LPL activity per cell and cell size were highly correlated. However, when differences in cell size were corrected for, no significant effect of genotype existed. Cardiac LPL activities were different between the two genotypes only in nondiabetic rats. These results suggested that both insulin and some other genetic factors were important in elevating adipose LPL activities and thus fat deposition in obese Zucker rats.
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PMID:Adipose lipoprotein lipase in insulin-treated diabetic lean and obese Zucker rats. 704 62

The present study was undertaken to determine whether exercise-training done in combination with feeding a high energy diet could modulate carbohydrate metabolism. Male rats were divided into exercise-trained or sedentary groups that received either a palatable high energy diet or merely standard laboratory diet. After 10 weeks of training, the animals were subjected to an intravenous glucose tolerance test. Body weight, epididymal fat pads, and adipocyte volume were reduced following training. The results also showed that exercise-training protects against deterioration of glucose tolerance produced by high energy diet. Training prevented the elevation of basal as well as glucose challenged insulin levels induced by the high energy diet in spite of a high fat as well as high overall energy intake. A highly significant coefficient of correlation (r = 0.78, P less than 0.01) was observed between the size of adipocytes and the insulin response to glucose load and suggests that the prevention of hyperinsulinemia in rats fed high energy foods while training could be associated with the ability to prevent obesity.
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PMID:Role of exercise-training in the prevention of hyperinsulinemia caused by high energy diet. 710 41

Young male Zucker lean (Fa/-) and obese (fa/fa) rats were fed the alpha-adrenergic blocking agent phenoxybenzamine as a dietary admixture for 35 days. In lean and obese rats, phenoxybenzamine treatment decreased significantly body weight gain, food consumption, grams of carcass fat, and grams of carcass protein. Lean rats exhibited reduced fat cell size and number in retroperitoneal, epididymal, and inguinal fat depots. Obese rats treated with phenoxybenzamine exhibited significantly decreased numbers of fat cells in the retroperitoneal, epididymal, and inguinal fat depots and a small decreased cell size in the inguinal fat depot only. The levels of carcass fat and protein and fat cell number in obese and lean rats treated with phenoxybenzamine for 35 days were similar to pretreatment values in agreement with the lack of body weight gain. Although values in agreement with the lack of body weight gain. Although rats exhibited marked decreases in fat accumulation during phenoxybenzamine treatment, fat cell size and number returned to control values during the posttreatment period with a marked hyperplasia occurring particularly in the retroperitoneal fat depot of obese rats. Serum levels of insulin were suppressed and free fatty acid levels increased in obese rats during phenoxybenzamine treatment, suggesting a stimulation of the sympathoadrenal system. This study shows that despite severe restrictions in fat cell proliferation during the rapid-growth phase of the obese Zucker rat, the mechanisms for cellular proliferation and fat deposition remain intact.
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PMID:Effect of phenoxybenzamine on development of adipose tissue in lean and obese Zucker rats. 713 43

Expression of the obese (ob) gene is augmented in the adipose tissue in several rodent models of genetic obesity. In the present study, we examined the ob gene expression in a rodent model of acquired obesity obtained by pure overfeeding of normal rats. Male Sprague-Dawley rats at 8 weeks of age were fed standard diet or high-fat diet. Rats fed high-fat diet developed moderate degree of obesity, hyperglycemia, and hyperlipidemia as compared with rats fed standard diet. Northern blot analysis revealed that the ob gene is expressed abundantly in the adipose tissue obtained from the epididymal, mesenteric, subcutaneous, retroperitoneal, and interscapular fat pads in rats fed standard diet. Expression of the ob gene was augmented in all the adipose tissue examined in rats fed high-fat diet. The present study demonstrates that the ob gene expression is augmented in the adipose tissue in diet-induced obesity, thereby suggesting the pathophysiologic roles of the ob gene in acquired obesity.
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PMID:Augmented expression of the obese gene in the adipose tissue from rats fed high-fat diet. 748 12

The effect of 1 wk of glucocorticoid deprivation by surgical adrenalectomy (ADX) on tissue 2-deoxy(-)[U-14C]glucose (2-DG) uptake and hepatic glucose production (HGP) was assessed in conscious, catheterized mice 5 wk after the induction of obesity with gold thioglucose (GTG). Despite the prevailing hyperglycemia and hyperinsulinemia, glucose uptake by heart, quadriceps muscle, and interscapular brown adipose tissue (BAT) of GTG-obese mice was unchanged compared with controls, suggesting that the hyperglycemia of GTG-obese mice is able to compensate for the insulin resistance of these tissues. In contrast, epididymal white adipose tissue (WAT) of GTG-obese mice showed increased glucose uptake with hyperglycemia and hyperinsulinemia. ADX decreased the hyperglycemia and lowered the elevated glycogen content of the liver of GTG-obese mice. ADX reduced glucose uptake by heart and WAT of control and GTG-obese mice, consistent with the concomitant decrease in insulinemia. Glucose uptake by muscle of control and GTG-obese mice was not significantly decreased after ADX despite the decrease in insulin, and ADX increased glucose uptake by BAT of GTG-obese mice, suggesting increased sympathetically mediated thermogenesis in this tissue. HGP was increased in GTG-obese mice compared with controls, and ADX significantly reduced HGP in both GTG-obese and control mice. These results suggest that the improved glucose tolerance of ADX GTG-obese mice and ADX control mice is due to a decrease in HGP rather than an increase in peripheral glucose uptake.
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PMID:Glucocorticoid deprivation alters in vivo glucose uptake by muscle and adipose tissues of GTG-obese mice. 749 45


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