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

A connecting link between carbohydrate and fat metabolism in adipose tissue is theconcentration of alpha-glycerophosphate derived predominantly from the glycolysis ofglucose entering the fat cell. However, several investigators have reported the presence of a glycerol specific kinase in the epidiymal fat-pad of the rat and obob mouse. This enzyme's presence in other mammalian adipose tissue could contribute to the alpha-glycerophosphate pool and thus affect both carbohydrate and fat metabolism within the fat cell. Glycerokinase was demonstrated in isolated fat cells obtained from the subcutaneous, perirenal, epididymal, and dorsal intrascapular brown fat depots of the adultmale rat. It was found to be particularly sensitive to in vivo lipogenic stimuli in both the subcutaneous and the brown adipose tissue and concluded that insulin is involved in adipose glycerokinase stimulation. Therefore, the main function of glycerokinase in normal adipose tissue may be to augment the anabolic action of insulin. It isfurther suggested that deviation from the normal control of this lipogenic enzyme couldlead to a gradual accumulation of fat and eventual obesity.
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PMID:Glycerokinase in mammalian adipose tissue: stimulation by lipogenic substances. 16 85

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

Thymidine kinase activity and the pattern of DNA accretion in the genetically obese Zucker rat (fafa) were shown to develop in a manner fundamentally different from that of the lean rat. In normal lean Zucker rats, fat cell size and number, thymidine kinase activity, total DNA, and DNA in lipid-filled and nonlipid-filled tissue changed as previously reported for the normally growing lean Sprague-Dawley rat. In the epididymal depot of the developing obese rat, the progressive obesity is characterized by marked early enlargement of fat cell size, elevated thymidine kinase activity until 273 days of age, increased rate of total tissue DNA accretion until 182 days of age, and fat cell hyperplasia that becomes manifest after an apparent "peak" cell size is reached at 98 days of age.
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PMID:Developmental changes in thymidine kinase, DNA, and fat cellularity in Zucker rats. 44 70

The purpose of this study was to determine if the elevated concentration of norepinephrine in the hypothalamus of the obese-hyperglycemic mouse plays a role in the development of this syndrome. We treated normal and obese mice with the monoamine oxidase inhibitors pargyline or clorgyline for 25 weeks. This resulted in significant inhibition of monoamine oxidase in their hypothalamus, cerebral cortex, kidney, heart and epididymal fat. There was a significant increase in the norepinephrine concentration of the hypothalamus of the normal mice and the cerebral cortex of the obese mice. The obese mice receiving clorgyline had an increase in plasma glucose (313 +/- 9 mg/dl). However, the increase in tissue norepinephrine concentration did not result in increased weight gain or alterations in organ weights in the mice. Thus, the elevated hypothalamic norepinephrine concentration in obese mice is probably not the cause of their obesity.
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PMID:The role of altered tissue norepinephrine concentration in the hereditary obese-hyperglycemic syndrome of mice. 52 84

Metabolic adaptations to cyclic patterns of food intake were studied in genetically lean and obese Zucker rats. Twenty-four lean and 24 obese rats were exposed to 12 hours of light and 12 hours of dark and allowed food ad libitum. Both groups of rats ate more during the dark period of the cycle. The obese consumed nearly twice as much food as the lean during the light period of the cycle. At 4-hour intervals, rats were killed and liver and epididymal fat pads were removed for metabolic studies. Adipose tissue from lean rats demonstrated marked changes in rates of lipogenesis during the 24-hour cycle whereas adipose tissue from obese rats maintained a relatively steady rate of lipogenesis. Glucose incorporation into the glycerol moiety of triacylglycerol was nearly 3-fold higher in adipose tissue from obese rats. Liver lipogenesis in lean and obese rats followed their food intake pattern. Liver lipogenic rate (expressed per organ) was 3- to 5-fold higher in obese than lean rats during most of the 24-hour cycle. These data support the concept that the excessive fatty acids produced in the liver of obese rats are being esterified by adipose cells. Lipolytic response to glucagon was found in adipose tissue from obese rats during the dark and light periods, but only during the dark period for lean rats. These data suggest, in comparison to lean rats, that obese rats do not enter a relative catabolic state during a 24-hour cycle. A constant anabolic state in the genetically prone individual may lead to excessive lipid deposition and obesity.
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PMID:Diurnal changes in adipose and liver tissue metabolism of lean and obese Zucker rats. 57 Oct 11

Male mice from a line selected for rapid postweaning growth (M16) and an unselected control (ICR) were reared from birth to 3 weeks either in litters of eight (N8) or 14 (N14). Body weight gain and feed intake of M16 mice were greater than ICR. These high rates of gain and feed intake also were extended to an older age in M16 (10 weeks) than in ICR (6 weeks). The M16 line exceeded the ICR line and N8 mice exceeded N14 for fat, lean, ash, and live body weights at 4, 6, 10, 16, and 30 weeks of age. Fat percentage was greater in N8 than N14 for both ICR and M16. The adipose cellularity of the epididymal fat pads of M16 indicated a hypertrophic-hyperplastic form of obesity at 10, 16, and 30 weeks. Within each line, the N14 mice had fewer and slightly smaller fat cells than N8. However, M16-N14 mice still had considerably more and larger fat cells than ICR-N8. Restriction of energy intake from birth to 3 weeks reduced subsequent feed intake and degree of obesity. After 4 weeks, the genetic effect exerted a greater influence on the development of obesity than the preweaning nutritional regimen.
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PMID:Adipose cellularity and body composition in polygenic obese mice as influenced by preweaning nutrition. 70 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

Lipoprotein lipase (LPL) enzyme activity in epididymal adipose tissue from obese and lean Zucker rats was measured. At 5, 10, 13, and 20 wk of age obese rats have heavier fat pads, larger fat cells, and more LPL per epididymal fat pad and per fat cell than do their lean littermate controls. Although LPL per fat cell increased as fat cell size increased in lean rats, the increased LPL activity in the obese could not be attributed solely to increased fat cell size. When obese and lean rats had similar cell sizes, LPL per fat cell was still significantly increased in the obese compared to lean. Furthermore LPL activity was increased in "preobese" (fa/fa) rats compared to either lean genotype (Fa/fa or Fa/Fa) during the second postnatal week. The data suggest that early increments in LPL activity in adipose tissue of the "pre-obese" rat may significantly contribute to the early fat cell hypertrophy seen during the development of this genetic obesity. Furthermore, early increased LPL activity may prove useful as a predictor of the onset of obesity.
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PMID:Increased adipose tissue lipoprotein lipase activity during the development of the genetically obese rat (fa/fa). 72 44

Wistar rats, 24 weeks of age, with alimentary obesity after fat feeding (50% fat in the diet) for 19 weeks were restricted to fat (3% fat in the diet) for 4 weeks in order to compare the alterations of body and organ weights as well as those of lipid concentrations in epididymal adipose tissue, liver and serum with earlier results [1], obtained before food changing. On these conditions decreases of body weight by about 20%, of the relative mass of epididymal adipose tissue and of the triglyceride content per fat cell were observed. In liver a decline of triglycerides and cholesterylesters (by about 2/3 and 1/3, respectively) and in serum a drop of free fatty acids, but increases of phospholipids, and of free and esterified cholesterol were found. In another series, animals of the same age that had been fed the low fat diet for 19 weeks were administered the high fat diet for 4 weeks and also compared with the state before. Thereby the body weight (by about 20%) and the relative mass of the epididymal adipose tissue gained, but lipid concentrations in this tissue were not affected. In liver the concentrations of triglycerides and cholesteryl esters increased threefold and tenfold, respectively; in serum augmented contents of triglycerides and phospholipids were observed. Besides the changes in adipose tissue, reasons for the forced accumulation of cholesteryl esters in the liver during fat feeding and their retarded removal out of the liver after fat restriction are especially discussed in comparison with that of the triglycerides.
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PMID:[Changes in lipid metabolism of Wistar rats by changing a high fat to a low fat diet and vice versa]. 75 10

The deposition of edidymal and perirenal fat, serum insulin levels, and insulin sensitivity of epididymal fat, expressed as the insulin-stimulated production of CO2 from glucose, were determined in Wistar rats fed diets containing either 54% starch or sucrose ad libitum or pair-fed in meals. Regardless of the pattern of feeding, sucrose-fed rats deposited more adipose tissue per 100 g body weight and exhibited less insulin sensitivity than did starch-fed rats. Significant differences in adipose tissue weights were not always accompanied by significant differences in body weights. Meal-fed rats deposited less adipose tissue and showed a greater insulin sensitivity than did ad libitum rats fed the same carbohydrate. However, when changes in feeding pattern negated the difference in adipose weights there was no difference in the insulin sensitivity of the meal-fed and ad libitum-fed rats. Rats consuming the sucrose diet generally exhibited significantly higher fasting serum insulin levels than did rats consuming the starch diet. The serum insulin values tended to be higher in the ad libitum-fpididymal tissue from the meal-fed and starch-fed rats tended to be greater than that of the sucrose-fed or ad libitum-fed rats, respectively, suggesting differences in adipocyte composition. Since obesity, insulin insensitivity, and hyperinsulinism are associated with an impairment of glucose tolerance, the observed metabolic effects of dietary sucrose are considered to be undesirable.
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PMID:Insulin sensitivity and adipose tissue weight of rats fed starch or sucrose diets ad libitum or in meals. 83 76


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