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

Diet-induced obesity in rats can be produced by high-fat feeding. Comparing high-fat with low-fat feeding, the present study was designed to characterize the phases of development of obesity. In the dynamic phase, male rats were investigated at the age of 9-10 weeks after feeding the diets for 4-5 weeks. In the static phase, the animals at the age of 24-26 weeks were tested after 20-22 weeks of the nutritional regime. In this phase, the effects of switching high-fat to low-fat diet for 4 weeks were also examined. Fractionating lipid extracts by thin layer chromatography the concentrations of several lipids in epididymal adipose tissue, in serum, and in liver were determined. In liver, the enhancement of cholesteryl-ester (CE) concentration after high-fat feeding besides the accumulation of triglycerides (TG) is remarkable. Cell fractionation studies of the livers by differential ultracentrifugation showed the major part of the accumulated CE in the supernatant. In vitro incorporation of (1-14C)acetate and (2-14C)mevalonate into liver slices indicated that cholesterol synthesis in the liver of the obese rats was not increased. Although the offered fat diet with 0.1% of cholesterol can not be considered as high in cholesterol, the 2.5-fold higher amount of the high-fat diet in comparison with the low-fat diet (0.04% cholesterol) could be responsible for the enlargement of CE in the liver of the fat fed rats. This possibility was proved by measurement of the cholesterol absorption and transport to the liver after oral administration of (4-14C)cholesterol. Estimation of TG secretion rates of the liver using Triton WR 1339 pointed out higher rates in the obese rats in the dynamic phase. In the static phase, the rates were not different between both feeding groups, while fat restriction in the food produced a striking increase of TG secretion. It is assumed that only in the dynamic phase metabolism is able to compensate the liver TG accumulation by an enhanced transport to the adipose tissue. In the static phase this ability is diminished but not lost.
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PMID:Some aspects of lipid metabolism in the liver of Wistar rats with fat diet-induced obesity. 403 42

Feeding rats with a cafeteria diet resulted in increases in total body weight and in epididymal-adipose-tissue weight. Those rats excreted significantly less N than did controls. The amount of N ingested by cafeteria-diet-fed rats was kept equal to that of controls. This decrease in N excretion is explained by a decrease in urinary excretion of urea. This may be due to the following facts. The rate of synthesis of urea from precursors by isolated hepatocytes from cafeteria-diet-fed rats was lower than in controls. In cafeteria-diet-fed rats the activities of all the enzymes of the urea cycle are decreased. The major percentage decreases are those of carbamoylphosphate synthetase (EC 6.3.4.16) and of argininosuccinate synthetase (EC 6.3.4.5), the enzymes probably involved in the regulation of the overall rate of the cycle. When rats are switched to normal chow diet, the enzyme activities return to normal values. The uptake of amino acids by liver of cafeteria-diet-fed rats is lower than in controls. These results contrast with those obtained previously by using other models of obesity in rat (i.e. genetic or hypothalamic), in which N excretion was increased.
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PMID:Decreased urea synthesis in cafeteria-diet-induced obesity in the rat. 406 72

There is a 'futile' cycle of unknown significance operating at a very rapid rate (about 40 percent that of the total central fat droplet's daily turnover rate) in white adipose tissue of normal mice. The futile cycle may be measured and studied because it occurs in a region of the adipose tissue that has poor anatomical contact with the capillaries coupled with a high affinity of the adipocytes, plasma membranes for the FFA in the ECF. The cycle is drastically inhibited in mice bearing the Ehrlich ascites carcinoma, a transplantable tumor; the inhibition is associated with a 20-fold increase in the FFA pool size of the epididymal fat pad (measured directly) and a 70 percent reduction in the TGFA pool that is involved in the cycle (estimated indirectly from kinetic measurements). However, the mass of TGFA in the central lipid droplet was being conserved in the tumor-bearing mice during this study. The TGFA pool involved in the cycle represents only about 1 percent of the total adipose tissue TGFA. The relation of this futile cycle to adipose TGFA turnover, plasma FFA turnover and oxidation to CO2, dietary sources of TGFA, and the loss (and preservation) of body fat in cancer-bearing animals was considered in terms of a simple model. Although the significance of the altered futile cycle is unknown, the new approach described here, coupled with other quantitative tracer and non-tracer measurements, may prove useful in understanding factors that lead to obesity or body fat loss.
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PMID:In vivo tracer studies of perturbed fatty acid transport and metabolism in adipose tissue. 406 21

Adipocyte cell size and number of three adipose depots, gonadal, subcutaneous, and retroperitoneal, were determined in several strains (aA(y), aA(iy), dbdb, obob, and NZO) of adult genetically obese mice, male and female, and in male gold thioglucose-treated mice. Epididymal pad cellularity was determined during development in yellow and viable yellow obese mice and their lean littermates, as well as in the NCS/R mouse. Cell number in the mouse epididymal pad in both lean and genetically obese animals is determined early in development, i.e., before weaning. Cell enlargement is the consistent and usually dominant morphological explanation for adipose depot enlargement in genetic and in gold thioglucose-induced mouse obesity. In some instances, hyperplasia accompanied the hypertrophy, occurring most often in the subcutaneous depot. Cell number in the subcutaneous pad of the obese-hyperglycemic female is four times that of the lean control and represents the most extreme case of hyperplasia observed. In fact, hyperplasia was consistently seen in the obob mouse. A classification for genetic obesity based primarily upon the cellularity characteristics of the adipose depots is proposed.
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PMID:Cellularity of adipose depots in six strains of genetically obese mice. 505 96

Cell size and number of three adipose depots, epididymal, retroperitoneal, and subcutaneous, were determined during growth of the obese Zucker rat ("fatty") and nonobese Zucker control. Cellularity of these depots in the adult "fatty" was compared with that in nonobese controls and in nonobese Zucker rats made obese by ventromedial hypothalamic lesions. Epididymal and retroperitoneal depots in the nonobese rat grew by cell enlargement and increase in cell number until the 14th wk, when number became fixed; further increase in depot size occurred by cell enlargement. The subcutaneous depot added cells until the 26th wk. In the Zucker "fatty," cell number increased until the 26th wk in all depots, accompanied by extreme cell enlargement. The enlarged adipose depots of the adult Zucker "fatty," when compared with the nonobese control, are the result of both hypertrophy and hyperplasia. Depot enlargement in the lesioned animal is the result of hypertrophy. "Fatties" have more cells in adipose depots than do lesioned rats. Genetic obesity in the Zucker rat is clearly different from the obesity produced by hypothalamic lesioning.
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PMID:Cellularity of adipose depots in the genetically obese Zucker rat. 512 35

The effect of infantile nutritional levels on adipose tissue cellularity and metabolism was studied in two groups of Sprague-Dawley rats. Caloric intake was varied during the suckling period by manipulating litter size immediately after birth; however, all animals had free access to food after weaning. The epididymal fat pads of animals raised in small litters were heavier than those of their paired siblings raised in large litters. Initially, the differences in pad weight were accounted for primarily by differences in total cell number; however, at 20 wk both cell number and cell size contributed equally. The rate of glucose incorporation into CO(2) and triglyceride during in vitro incubations was the same for both groups if expressed on a per cell basis; therefore total tissue incorporation was greater in animals with more cells. The results support the hypothesis that early nutritional experiences can effect permanent changes in the cell number and size of the epididymal fat depot and that total cell number is important in the total metabolism of this organ. These findings and the fact that extreme human obesity is accompanied by similar alterations in cellularity and metabolism indicate that early nutritional experiences should be studied further as a guide to the etiology of obesity in man.
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PMID:Effect of early nutrition on the development of rat epididymal fat pads: cellularity and metabolism. 567 29

The presence of a lipidbound inhibitor in adipose tissue of rats with hypothalamic obesity may explain the failure of the tissue to release fatty acids on epinephrine stinmulation. Aqueous extracts of tissue from obese animals showed no deficiency of lipase activity, but when whole homogenates of epididymal fat from lean and obese animals were mixed, 25 percent tissue from obese animals reduced by 73 percent the release expected from tissue of lean controls.
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PMID:Lipolysis in homogenates of adipose tissue: an inhibitor found in fat from obese rats. 600 38

Synthesis of fatty acids was measured in the liver and in epididymal adipose tissue of sand rats and albino rats. In chow-fed sand rats the rate of hepatic lipogenesis, as measured by the incorporation of 3H2O into fatty acids, was four- to sevenfold higher than in albino rats and in sand rats on a low-calorie saltbush diet. The contribution of [14C]glucose to lipogenesis in sand rat liver was lower than in albino rats. In fed sand rats lipogenesis incorporating 3H2O was stimulated by casein but not by glucose. In adipose tissue, lipogenesis measured 1 h after administration of 3H2O was much lower in sand rats than in albino rats. In vitro incorporation of [14C]glucose or acetate into adipose tissue fatty acids was negligible. In adipose tissue, uptake of very-low-density lipoproteins (VLDL) and lipoprotein lipase activity were sevenfold higher than in albino rats. Activities of NADP-malate dehydrogenase, acetyl CoA carboxylase, and fatty acid synthetase were considerably higher in the liver of chow-fed sand rats than in albino rats. It was concluded that obesity in sand rats originates from hepatic lipogenesis without a significant contribution of local fatty acid synthesis in adipose tissue.
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PMID:Lipogenesis in the sand rat (Psammomys obesus). 634 15

Chronic uraemic rats had decreased food intake, and this was accompanied by decreased weight of the epididymal fat-pads and interscapular brown adipose tissue. Normal rats whose food intake was restricted to an amount similar to that of the uraemic rats showed similar decreases in weight of the adipose-tissue depots. In addition, the food-restricted rats had decreased liver weight compared with normal or uraemic rats. The basal rate of lipogenesis was decreased in liver and epididymal fat-pads of food-restricted and uraemic rats and in interscapular brown adipose tissue of uraemic rats. Administration of a low-glucose-containing (1.36%) peritoneal-dialysis solution slightly increased lipogenesis in liver of uraemic rats, but had no significant effect in epididymal fat-pads. For brown fat, the rate of lipogenesis was increased in normal, food-restricted and uraemic groups, but the values for the last group were 4-5-fold lower than for the food-restricted or control groups. A high-glucose-containing (3.86%) peritoneal-dialysis solution gave similar rates of lipogenesis in liver, epididymal fat-pads and brown fat of all three groups, but for brown fat moderately uraemic rats showed a considerably lower rate of lipogenesis than did mildly uraemic rats. The basal plasma insulin concentration was lower in the food-restricted (50%) and uraemic (70%) groups than in the control group. The low-glucose peritoneal-dialysis solution increased plasma insulin to control values in the food-restricted rats, but had no significant effect on plasma insulin in the uraemic rats, despite a significant increase in blood glucose in this group. It is concluded that there is an impairment of the lipogenic response to intraperitoneal glucose loads in interscapular brown adipose tissue of uraemic rats, and that this is not due to the accompanying decrease in food intake. The hypoinsulinaemia may be an important factor. The possible relevance of this finding to the obesity observed in some uraemic patients treated by peritoneal dialysis with glucose-containing solutions is discussed.
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PMID:Effects of glucose-containing peritoneal-dialysis solutions on rates of lipogenesis in vivo in the liver, brown and white adipose tissue of chronic uraemic rats. 635 52

The influence of gastric inhibitory polypeptide (GIP) on fatty acid incorporation into adipose tissue (FIAT) was studied in the rat on epididymal fat pads at concentrations amounting to 1, 2 and 4 ng/ml. Without insulin in the incubation medium, GIP induced a slight though significant FIAT decrease with a maximum of 9% for 2 ng/ml concentration. In the presence of rat insulin (100 microU/ml), it significantly enhanced the insulin-induced FIAT increase, that progressed from 106.4% of the basal value to 110.5% for 1 ng/ml concentration (P less than 0.025) and to 118.2% for 4 ng/ml concentration (P less than 0.0025). The existence of such a phenomenon as well as that of an hyperactive enteroinsular axis in obese subjects could represent two important factors in the development of obesity.
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PMID:Gastric inhibitory polypeptide enhancement of the insulin effect on fatty acid incorporation into adipose tissue in the rat. 635 87


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