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

A rat model for severe obesity has been developed by feeding the animals a fat-rich, sugar-rich diet. The concentration of fat in the diet was similar to what most Americans consume (about 40% kcal from fat). Calories from sugar was calculated to be 40.6%. As adults, body fat content in these animals averaged 61 or 51%, depending on whether the fat-rich, sugar-rich diet caused hyperphagia. The rate of body fat accretion in these severely obese rats raised in litters of four was estimated to be 1.78 +/- 0.12 (SE) g X d-1 (61% body fat) or 0.9 +/- 0.03 g X d-1 (51% body fat). In contrast, lean rats eating a diet of Purina chow deposited fat at a rate of 0.20 +/- 0.02 g X d-1, resulting in a carcass fat content of 18%. Preliminary evidence based on adult body weights of sugar-fed rats suggests that sucrose alone can cause severe obesity similar to that seen with dietary fat alone. Currently, an attempt is being made to determine how dietary fat and/or dietary sugar work to produce severe obesity. One possibility is that dietary fat in the form of a chylomicron and dietary sugar in the form of a very low density lipoprotein may modify adipose tissue lipoprotein lipase activity. This enzyme acts as a gatekeeper for circulating triglycerides entering the adipocyte. It is our belief that the results obtained will help to lay the groundwork for determination of the role of exercise in weight control.
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PMID:Dietary-induced severe obesity: exercise implications. 395 65

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

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

The proper understanding of obesity requires a multifaceted approach. Behavioral considerations of eating and activity patterns do not account for the large between- and within-subjects variance associated with the energy-balance equation. Sources of adaptive and dispositional variance in metabolic rates are reviewed and suggested to be a likely source of importance for the proper conceptualization and intervention of obesity. Five proposed mechanisms of metabolic variation are reviewed with consideration of the supporting evidence for each mechanism. The generalizability of some of the proposed mechanisms is limited because of the scope of past research. However, the roles of lipoprotein lipase in fat storage and brown adipose tissue in thermogenesis are intriguing possibilities for future research with humans.
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PMID:Mechanisms of energy balance in obesity. 632 42

Obesity was induced in male Sprague-Dawley rats by overfeeding a cafeteria-style diet. The obesity was characterized by both adipocyte hypertrophy and hyperplasia. Body weight was then reduced by starvation to match that of control animals that had been fed ordinary Purina Chow. The previously obese rats were then refed to match the same body weight as controls, or given the same amount of Purina Chow as consumed by the controls. This resulted in a remaining moderate obesity, now due only to adipocyte hyperplasia with normal fat cell size. The previously obese rats needed less energy to keep their body weight equal to controls, and they spontaneously ate less than controls. They were, however, less food efficient because they did not accumulate as much energy in fat and protein depots during the period of refeeding as the controls did, and consequently must have transformed more energy into heat. This is in sharp contrast to nonobese animals subjected to a similar experimental procedure. Lipogenic enzymes and lipoprotein lipase activity in adipose tissue as well as plasma insulin concentrations were elevated in overfed rats but normalized during refeeding of Chow after fasting.
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PMID:Refeeding after fasting in the rat: effects of dietary-induced obesity on energy balance regulation. 633 94

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

The basal rate of lipolysis and basal lipoprotein lipase activity were determined in vitro in subcutaneous adipose tissue obtained from eight healthy non-obese subjects, ten obese subjects before and during one week's starvation, nine untreated non-insulin dependent diabetics and seven treated non-insulin dependent diabetics whose disease had been under metabolic control for at least three months. There was a negative correlation between the rate of lipolysis and activity of lipoprotein lipase in untreated diabetes mellitus and during starvation (r from -0.87 to -0.81). Under these two conditions the rate of lipolysis is increased and the lipoprotein lipase activity is decreased. There was no correlation between lipolysis and lipoprotein lipase in non-obese subjects, non-starving obese subjects and treated diabetic patients (r from 0.11 to 0.36). Thus, during starvation and in untreated diabetes, there is a strong reciprocal relationship between basal lipolytic activity and basal lipoprotein lipase activity in human adipose tissue which is not found under normal conditions or in obesity and well-controlled diabetes. It is concluded that a negative connection between lipolysis and lipoprotein lipase in human adipose tissue may be of physiological importance for the regulation of the energy balance in conditions such as untreated non-insulin dependent diabetes and starvation where adipose tissue lipids are the major source of energy.
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PMID:The relationship between the basal lipolytic and lipoprotein lipase activities in human adipose tissue. 634 23

The effects of treatment on plasma total triglyceride, total cholesterol, and plasma postheparin lipase activities have not been evaluated in non-insulin-dependent diabetic (NIDD) subjects without a coexisting familial lipid disorder. In 49 untreated NIDD subjects, there was a linear relationship between glycosylated hemoglobin (GHb) and triglyceride (r = 0.35, P less than 0.02). This correlation was improved after adjusting for the effects of obesity by a partial correlation analysis. After therapy, there was a significant relationship between the change in GHb and the change in triglyceride. To determine whether changes in lipid removal from plasma may contribute to the decrease in plasma lipid concentrations during treatment, the plasma postheparin lipoprotein lipase and hepatic lipase activities were evaluated in a subgroup (N = 8) of these NIDD subjects before and after 1 and 3 mo of therapy. Plasma postheparin hepatic lipase activity in the NIDD subjects was not different from that observed in six normal control subjects and did not change during therapy. In contrast, plasma postheparin lipoprotein lipase activity was lower in the untreated NIDD subjects than in the control subjects. Analysis of the two phases (early and late) of the postheparin lipoprotein lipase activity in plasma showed that the abnormal early phase in untreated NIDD corrected to normal values in less than a month, but the late phase was not corrected until the 3-mo measurement. These findings suggest that some NIDD subjects have a defect in heparin releasable lipoprotein lipase activity, which is reversed with improved glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The response of plasma triglyceride, cholesterol, and lipoprotein lipase to treatment in non-insulin-dependent diabetic subjects without familial hypertriglyceridemia. 635 82

Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 +/- 2.0 (+/- SEM) and 9.6 +/- 2.7 neq/g X min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P less than 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 +/- 1.3 ngq/g X min; P = 0.01), whereas the obese group did not (2.3 +/- 1.9 neq/g X min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 +/- 6.5 neq/g X min; P = 0.01) and obese subjects (9.8 +/- 2.3; P less than 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 10(6) cells. Basal ATLPL per 10(6) cells [11.8 +/- 1.7 neq/10(6) cells X min (obese); 3.4 +/- 0.9 neq/10(6) cells X min (normal)] was a function of cell size (rs = 0.713; P less than 0.001), body mass index (rs = 0.565; P less than 0.005), and basal insulin levels (rs = 0.434; P less than 0.05). As with the ATLPL per g response, the increases in ATLPL per 10(6) cells above basal were significant at both the 3 and 6 h marks for the normal subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 +/- 24 microU/ml (obese); 251 +/- 27 microU/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 +/- 23 mg/m2 X min (obese); 312 +/- 33 mg/m2 X min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.
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PMID:Insulin responsiveness of adipose tissue lipoprotein lipase is delayed but preserved in obesity. 638 39

At any age, with increases in body weight, the elevation in total lipid or abdominal fat is more than proportional to body weight. This observation explains why selection of broilers for rapid growth rate leads to excessive fat accumulation. Although adipocyte hyperplasia continues until 12 or 14 weeks of age, hypertrophia becomes increasingly important with age and the degree of fattening. The number of adipocytes appears to be correlated with body size, and the size of the adipocyte is closely related to the fat content of the live bird. The hormonal control of lipolysis involves a number of hormones and appears to be very complex. The increase in fat in adipose tissue is mainly due to hepatic lipogenesis. This review discusses the relative role of hormones in fat metabolism, some pecularities of insulin activity in birds, and the important functions of plasma lipoprotein and adipose lipoprotein lipase. A comparison of a fat line of chickens and mammalian models of obesity is also made.
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PMID:Adipose tissue metabolism and its control in birds. 638 92


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