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

The stroma vascular fraction of adipose tissue partly consists of adipose precursor cells which can convert into adipocytes in vitro. The aim of this study was to investigate the possible contribution of cells from the stroma vascular compartment to the initiation of obesity induced by overfeeding during the early neonatal weeks in rats. Overfeeding during the suckling period was obtained by reducing the litter size. The inguinal adipose tissue of overfed rats raised in litters of 4 pups each was overdeveloped compared to that of controls raised in litters of 8 pups each, and the difference between the two groups became significant as early as 10 days of age. At this age, adipose tissue enlargement was only due to adipocyte hypertrophy; afterwards, hyperplasia of the mature fat cells contributed to the overdevelopment of adipose tissue in 15-day old overfed rats. The cell number in the stroma vascular fraction increased in the overfed group as early as 10 days of age and thus preceded the onset of mature fat cell hyperplasia. The developmental pattern of lipoprotein lipase, glycerol-3-phosphate dehydrogenase, glycerol-acyl-transferase and acyl-CoA ligase activities in stromal cells did not depend on litter size, but specific enzyme activities wee increased in 10-day old overfed rats compared to the controls. These results indicate that early overfeeding induced cell proliferation in the stroma vascular compartment and also induced the enzyme activities involved in adipose conversion to increase in these cells. This strongly suggests that precursor cell differentiation was greater in overfed rats than in control rats.
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PMID:[Role of adipocyte precursors in the initiation of nutritional obesity before weaning]. 399 88

Five years after entry into a study prospective from diagnosis of non-insulin-dependent (Type 2) diabetes, 17 patients were known to be dead and 197 alive. On analysis of 136 patients (12 deaths) in whom there was complete information from clinical, metabolic and hormonal examination both before and 1 yr after start of treatment, an index of liability to death within this first 5 yr was calculated, to separate best the dead from the living. One index value correctly ascribed 83% of the dead and 90% of the living (89% of all predictions correct; Youden's "J" value = 0.73). Estimates from the less complete data on the other 78 patients (5 deaths) did not alter the predictive factors. Prediction is more successful with non-cardiac than with cardiac deaths. Five factors contributed to the predictive index for death. One was a long duration of symptoms as recalled at diagnosis. The other 4 factors all came from the 1-yr review (no death then). These were (a) greater glucose intolerance, as expressed by the KG rate constant for disappearance of i.v. injected glucose from the blood (more useful than fasting glucose concentration); (b) higher systolic blood pressure (more useful than diastolic); (c) less obesity, as expressed by the Body Mass Index, and (d) higher fasting blood glycerol concentration. As expected, hyper-glycaemia (as reflected in the KG value) is important, but adrenergic factors may contribute to (a), (b) and (d). From these results earlier diagnosis of this type of diabetes could well be associated with an improved outlook, and in addition this alone might ameliorate the other factors, but measures to normalise them post-diagnosis also require testing.
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PMID:Mortal factors in type 2 (NIDDM) diabetes mellitus. 399 73

The influence of obesity on the metabolism of apolipoprotein B (apo B) in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) was investigated in nine obese and seven nonobese Pima Indian men. Kinetics of VLDL-apo B (VLDL-B), VLDL-triglycerides, IDL-B and LDL-B were studied after injection of autologous 131I-VLDL, [3H]glycerol, and autologous 125I-LDL. Specific activities were measured in apo B isolated from all lipoprotein fractions and in triglyceride isolated from VLDL. Transport rates and fractional catabolic rates for apo B in VLDL, IDL, and LDL and triglyceride in VLDL were determined by multicompartmental analysis. This method also allowed the estimation of rates of interconversions of the lipoproteins. The two groups had similar mean ages and heights, but the obese group had a higher total body weight (131 +/- 14 vs. 66 +/- 3 kg +/- SEM) and fat free mass (81 +/- 5 vs. 54 +/- 2 kg) than lean controls. Plasma total lipids were similar for the two groups, and apo B concentrations in VLDL, IDL, and LDL were similar in obese and lean subjects. In spite of similarity in concentrations, obese subjects compared to lean subjects had higher synthetic rates of VLDL-triglyceride (62.6 +/- 15 vs. 26.2 +/- 7 g/d, P less than 0.01), VLDL-B (2,241 +/- 215 vs. 1,113 +/- 72 mg/d, P less than 0.001), and LDL-B (1,234 +/- 87 vs. 802 +/- 83 mg/d, P less than 0.01). Furthermore, in obese subjects, significantly higher amounts of VLDL-B were removed from the circulation without conversion to LDL-B (1,078 +/- 159 vs. 460 +/- 34 mg/d, P less than 0.05), and obese subjects had a higher fractional catabolic rate for LDL than the lean controls (0.48 +/- 0.02 vs. 0.41 +/- 0.02 d-1, P less than 0.05). The rapid catabolism of LDL and increased metabolism of VLDL without conversion to LDL in obese individuals may be mechanisms for maintenance of LDL at normal levels despite the overproduction of its precursor.
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PMID:Influence of obesity on the metabolism of apolipoprotein B in humans. 403 Oct 64

[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Incorporation of [1-(14)C]glucose into glyceride-fatty acids by these tissues could not be demonstrated under any of the conditions tested. Both adipose cell size and dietary composition influence the in vitro metabolism of glucose in, and the response to insulin by, human adipose tissue. During periods of ingestion of weight-maintenance isocaloric diets of similar carbohydrate, fat, and protein composition, increasing adipose cell size is associated with (a) unchanging rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet.The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible with weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.
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PMID:Glucose metabolism and the response to insulin by human adipose tissue in spontaneous and experimental obesity. Effects of dietary composition and adipose cell size. 481 43

Six grossly obese patients were fed 5000 calorie diets for 4 wk. During one period of 2 wk, the calories were consumed over 4 hr (gorging) and during the other 2 wk, the dietary intake was spread over 20 hr (nibbling). Each of these periods followed a low caloric intake which lasted at least 10 days. Three male patients (group I) were studied at or near their maximal weight and three females (group II) after a weight loss of 50-70 kg. The patients in group II gained more weight than those in group I. Lipogenesis from pyruvate was greater in group II than in group I. Rapid ingestion of food (gorging) was accompanied by a significant increase in glyceride-glycerol-(14)C and fatty acids-(14)C from pyruvate-(14)C. The enzymatic activity of sn-glycerol 3-phosphate dehydrogenase and mitochondrial glycerophosphate oxidase paralleled the rate of formation of glyceride-glycerol. Lipogenesis from pyruvate was significantly lower when the bicarbonate concentration was reduced from 25 to 10 mM. Citrate and acetate were also converted to fatty acids but there was no difference between gorging and nibbling. An inhibitor of carbonic anhydrase significantly reduced the conversion of pyruvate into CO(2), glyceride-glycerol, and fatty acids. These data on gorging and nibbling have been related to other studies suggesting that the frequency of food intake may be inversely related to obesity.
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PMID:Lipogenesis in human adipose tissue: some effects of nibbling and gorging. 501 Oct 99

Lipogenesis from glucose and lipolysis in human omental and subcutaneous fat cells were studied as functions of adipose cell size and number in adult females. Since subcutaneous fat cells were larger than those prepared from the greater omentum, a comparison could be made of the metabolism of different sizes of cells within individual subjects. Rates per cell of glyceride-glycerol and glyceride-fatty acid synthesis from glucose were similar in omental and subcutaneous fat cells incubated in the presence or absence of insulin. However, subcutaneous fat cells exhibited higher rates of basal lipolysis than omental fat cells and these differences were maintained when lipolysis was stimulated with theophylline. Different rates of lipolysis were not demonstrable after incubations with epinephrine, indicating that subcutaneous fat cells were less responsive to this hormone than smaller omental fat cells. Correlation and partial correlation analysis showed that differences in basal and theophylline-stimulated lipolysis between fat cells prepared from different subjects and between omental and subcutaneous fat cells could be accounted for by differences in adipose cell volume. In subcutaneous fat cells highly significant intercorrelations were demonstrated between cell volume, basal lipolysis, and the basal conversion of glucose to glyceride-glycerol. There was no correlation between fat cell volume, age, or relative obesity and the effects of theophylline or insulin on lipolysis or lipogenesis from glucose in vitro when the data were expressed as percentage changes above basal values.
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PMID:Lipolysis and lipogenesis from glucose in human fat cells of different sizes. Effects of insulin, epinephrine, and theophylline. 542 23

Subcutaneous fat cells were isolated from genetically obese rats and from rats with obesity produced by hypothalamic lesions. Insulin did not augment the oxidation of fatty acids or their synthesis from glucose-1-(14)C or glucose-1-(3)H by fat cells from either group. Radioactivity from pyruvate-3-(14)C was incorporated into fatty acids to the same degree by fat cells from these two groups. The presence of 5 mm glucose in the incubation medium containing fat cells and pyruvate-3-(14)C or aspartate-3-(14)C stimulated the synthesis of fatty acids to a greater extent in cells of genetically obese rats. Fasting, in contrast, reduced the incorporation of radioactivity from pyruvate and glucose into fatty acids by fat cells from the genetically obese animals. In all experiments the fat cells from genetically obese rats converted more radioactivity into glyceride-glycerol relative to CO(2) than did fat cells from hypothalamic obese rats. Parabiosis between one thin and one genetically obese litter mate was performed in three pairs of rats without influencing growth of either rat. Thus in the present studies fat cells from genetically obese rats showed two differences from normal fat cells: they channeled more radioactivity from pyruvate into fatty acids in the presence of glucose, and they uniformly converted more radioactivity into glyceride-glycerol.
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PMID:Lipogenesis from glucose and pyruvate in fat cells from genetically obese rats. 568 60

Neonatal sympathectomy with guanethidine (50 mg/kg for 3 wk) in Sprague-Dawley rats was previously shown not to significantly affect body weight gain, even when rats were raised in small litters and fed a high-calorie diet from weaning to produce diet-induced obesity (15). In our study rectal temperatures of cold-stressed (24 h at 4 degrees C) sympathectomized rats (obese and lean) fell only 1.4 degrees C after 4 h and were normal by 24 h, as were plasma catecholamine, glycerol glucose, and insulin levels after 4 h at 4 degrees C. Obese rats (with or without sympathectomy) had decreased 4-h (at 4 degrees C) plasma norepinephrine (NE) and increased basal and 4-h plasma glycerol, glucose, and insulin levels. Despite greater than 95% depletion of interscapular brown adipose tissue (IBAT) NE in sympathectomized rats, there was no alteration in beta-adrenoreceptor binding and only 10 and 32% decreases in basal and maximal NE-stimulated O2 consumption, respectively. Obese rats had significant increases in IBAT beta-receptor binding (148-190%/cell, 77-155%/pad) and in basal (11-19%) but not maximal O2 consumption. These results suggest that factors other than the sympathetic nervous system can effectively control thermoregulation, IBAT metabolism, and body weight in the presence of a chronic defect in sympathetic function.
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PMID:Dietary obesity and neonatal sympathectomy. II. Thermoregulation and brown adipose metabolism. 609 88

The insulin-like activity of the pituitary pars-intermedia insulin secretagogue beta-cell-tropin, ACTH22-39, has been studied on rat adipocytes. The peptide was prepared by tryptic digestion of synthetic human CLIP, ACTH18-39. beta-Cell-tropin stimulated the incorporation of 3H2O into total lipids. The 50% maximal activity concentration was 5 X 10(-2) ng/ml-1 about 2.5 X 10(-11) M. Iodination of tyrosine, the penultimate amino-acid of the N-terminal, eliminated lipogenic activity, and acetylation of the N-terminal valine reduced activity. ACTH and CLIP (ACTH18-39) had no lipogenic action on the adipocyte system studied. beta-Cell-tropin stimulated the oxidation of glucose and the conversion of glucose into saponified fatty acids and glyceride glycerol. The influence of beta-cell-tropin and insulin on the incorporation of glucose into total lipids, saponified fatty acids and glyceride glycerol was not additive. The results suggest that beta-cell-tropin is either a potent lipogenic hormone, stimulating the conversion of glucose into lipids or that it activates endogenous insulin. The biological activity is associated with the N-terminal amino-acids of the peptide. The possible significance of beta-cell-tropin in obesity is discussed.
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PMID:The insulin-like action of beta-cell-tropin on glucose and lipid metabolism in adipocytes. 609 18

The activity of the enzyme glycerokinase is low in mammalian adipose tissue, but high in certain forms of genetic obesity in rats and mice. This study was undertaken to determine if obese human subjects had higher glycerokinase activity than normal-weight subjects. Seventy-three randomly selected patients undergoing abdominal surgery were studied. Subcutaneous and omental adipose tissue was removed during surgery and the activity of the enzyme glycerokinase was measured in vitro under optimal conditions. The following observations were made: (1) the mean activity, when expressed per microgram DNA, was significantly (P less than 0.05) higher in obese subjects at both sites, yet no direct correlation to the degree of obesity was found; (2) the individual activity in morbidly obese patients undergoing gastroplasty correlated inversely with the rate of postoperative weight loss (r = -0.58, P less than 0.05); (3) glycerokinase activity was directly related (r = 0.59, P less than 0.01) to the rate of spontaneous glycerol release, and inversely related (r = -0.51, P less than .025) to the stimulation in glycerol release by norepinephrine; (4) the ratio glycerokinase/lipoprotein lipase in omental adipose tissue correlated with the degree of obesity (r = 0.43, P less than 0.05); (5) in nondiabetic male obese adults, the glycerokinase activity in subcutaneous adipose tissue inversely correlated with age (P = 0.05) and (6) the glycerokinase activity had two apparent Km values in three obese patients, in which it was studied kinetically. It is concluded that a small subsection of the obese population have a high potential for glycerol phosphorylation. In these individuals, weight loss is more difficult since they tend to reutilize the glycerol formed by lipolysis and net glycerokinase activity in their adipose tissue may reflect variations in lipid turnover.
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PMID:Glycerokinase activity in human adipose tissue as related to obesity. 609 31


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