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

The lipoprotein-lipase activity (LPLA) in the abdominal, subcutaneous, adipose tissue was studied in a random sample (n = 69) of 60-year-old men. A new method for the quantification of LPLA was applied. The mean value was 67 mU/g when expressed per gram (wet weight) of adipose tissue. Several subjects within the lower part of the range of adipose-tissue LPLA values had low concentrations of serum-triglycerides (S-TG). There was no correlation between the LPLA and S-TG concentrations in the fasting state. Among the 69 subjects, four had newly detected diabetes mellitus and had significantly lower LPLA in the adipose tissue than the control group. The fat-cell size and the LPLA per gram of adipose tissue were not correlated. Thus, obesity without diabetes mellitus does not imply a low LPLA concentration in adipose tissue. The variation of the concentration of adipose-tissue LPLA in the fasting state in this population was explained only to a minor extent by the variation of S-insulin and blood-glucose parameters, when analysed statistically by a stepwise multiple-regression technique.
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PMID:Lipoprotein-lipase activity in subcutaneous, adipose tissue in healthy subjects: variation of activity in a population of 60-year-old men. 3 Jan 95

Most of the many metabolic abnormalities associated with obesity are corrected by weight reduction. Adipose-tissue lipoprotein-lipase activity per cell is increased in obesity. Adipose-tissue lipoprotein-lipase was significantly higher in seven previously obese men studied at a stable reduced weight than in a control population. In fact, enzyme activity was significantly higher than would have been predicted from the obese men's maximum weight. These results indicate that abnormalities in adipose-tissue lipoprotein lipase may have a primary role in the development of obesity.
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PMID:Increased adipose-tissue lipoprotein-lipase activity in moderately obese men after weight reduction. 7 95

The activities of three lysosomal hydrolases were assayed in the basal and isoproterenol-stimulated states in the adipose tissues of lean, obese and obese-diabetic monkeys. The basal activity of acid lipase appeared higher in the obese tissues with or without diabetes than in the lean tissue. Isoproterenol stimulation did not affect these activities. The basal activity of beta-galactosidase (beta-Gal) was similar in all tissues and unaffected by isoproterenol stimulation. Although basal activity of hexosaminidase (Hex) was comparable in all tissues, activity increased significantly in the stimulated diabetic-obese tissue but not in the stimulated tissues from lean animals or animals with simple obesity.
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PMID:Catechol effect on the lysosomal enzymes in the adipose tissues of obese and obese-diabetic monkeys. 11 11

Tissue monoacylglycerols (MG), diacylglycerols (DG), free fatty acids (FFA), and cyclic AMP (cAMP) and release of FFA and glycerol have been studied in vitro in subcutaneous adipose tissue of 6 obese and 7 normal-weight subjects. The tissue was incubated without or with 6 X 10(-5) mol/l of isoprenaline (ISNA). The DG level and the fat cell volume were strongly interrelated (r=+0.95, p less than 0.001). The concentration of DG was increased (p less than 0.05) in obesity. The changes in DG and MG were significantly interrelated (r=+0.65, p less than 0.05) during basal incubation. ISNA increased the DG concentration in a way that was correlated (r=+0.81, p less than 0.001) with the ISNA-induced glycerol release. This indicates that 1) the basal metabolic activities of MG and DG lipase are similar and 2) DG lipase is an important rate limiting factor in lipolysis. Without ISNA, tissue FFA and the release of FFA and glycerol were significantly increased in the obese patients. As a mean, MG and DG did not accumulate in the basal state in the two patient groups. The findings indicate that basal lipolysis was increased in obesity. This was probably due to increased basal metabolic activity of triacylglycerol lipase, since the basal cAMP levels were similar in the two patient groups. In the presence of ISNA, the production of FFA and the glycerol release were similar in both patient groups, as was the increase in tissue DG. Also the ISNA-induced maximal level of cAMP was similar in the two groups. With ISNA, a small increment of MG was observed in adipose tissue of the normal-weight subjects. Taking all metabolites into account, the rate of lipolysis as well as the activation of triacylglycerol lipase via cAMP in the presence of ISNA appeared to be unaltered in obesity. Separate experiments with 1-14C-glycerol provided further evidence for the existence of a MG pathway for the esterification of FFA.
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PMID:Metabolism of mono- and diacylglycerols in subcutaneous adipose tissue of obese and normal-weight subjects. 18 90

Based on the consideration that insulin does not act directly on metabolic processes but affects membrane carriers and key-enzymes that regulate metabolic pathways, determination of insulin responsiveness of the various key-enzymes is suggested as a very appropriate method for studying insulin resistance. Insulin resistance, as it occurs in obese or obese-diabetic humans and animals, is most often associated with hyperinsulinemia, and is characterized not only by increased activity of key-enzymes of pathways known to be stimulated by insulin (glycolysis, lipogenesis), with the possible exception of glycogen synthesis, but also by a trend towards increased activity of key-enzymes of 'catabolic pathways', normally depressed by insulin. In the adipose tissue there is a normal-to-enhanced basal lipolysis, which in man would result from the prevalence of the active over the inactive form of triacylglycerol lipase. In muscle, the increased amino-acid release that can be inferred from the elevated blood level of both alanine and branched-chain amino acids suggests an enhanced proteolysis. In liver, there is an elevation in the activity of the key gluconeogenic enzymes, which forms the basis of the augmented gluconeogenesis. In both muscle and liver, phosphorylase is also elevated with no change in glycogen synthase. Therefore, insulin resistance seems to consist of the failure of insulin to depress the key-enzymes of catabolic pathways. Possible resistance of glycogen synthetase, which might account for decreased glucose utilization in muscle, may be due to the opposing effects of the phosphorylation process on glycogen synthetase and phosphorylase, implying that activation of phosphorylase (which occurs in obesity) entails inhibition of the synthetase. The fact that insulin insensitivity concerns only the 'catabolic' but not most 'anabolic' pathways makes it unlikely that the unresponsiveness is due to a reduction in insulin receptors or increase in insulin degradation. Since resistance to insulin is shown by enzymes regulated by such different mechanisms as induction-repression (gluconeogenic enzymes), covalent modifications (lipase, phosphorylase), and changes in lysosome stability (lysosomal proteases responsible for proteolysis, a single basic mechanism for explaining insulin insensitivity cannot be envisaged at present.
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PMID:Insulin resistance in obesity: a critical analysis at enzyme level. A review. 39 47

Seventy-seven chronic alcoholic subjects admitted to two alcoholic detoxification centers were evaluated for lipid abnormalities. Nineteen (26%) of these male patients had serum triglyceride levels greater than 150 mg/100 ml and six (9%) had serum cholesterol levels greater than 250 mg/100 ml. Compared to 33 age-matched, nonalcoholic control subjects, there was a significantly greater incidence of hypertriglyceridemia in the alcoholic subjects. All patients with triglyceride abnormalities had type IV electrophoretic patterns. The triglyceride elevations were not related to serum amylase, lipase, liver function, obesity, and abnormal fasting glucose. We conclude that there is a significant increase in hypertriglyceridemia in chronic alcoholic patients.
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PMID:Ethanol-induced hypertriglyceridemia. Prevalence and contributing factors. 63 36

Published studies have shown that overproduction of very low density lipoproteins is a major factor leading to hypertiglyceridemia in obesity. Few systematic studies of triglyceride removal or postheparin lipoprotein lipase activity (LPLA) in obesity have appeared. We have examined heparin-released lipoprotein triglyceride hydrolase activities in 12 lean and 12 obese age- and sex-matched volunteers after overnight fasting. Heparin doses were calculated to compensate for the disproportionality between body mass and plasma volume in obesity. Triglyceride hydrolase activities of hepatic (HTGLA) and extrahepatic (LPLA) origin were distinguished by in vitro inhibition of LPLA with protamine sulfate. Incremental heparin doses were given to each subject to determine lipase activities under conditions of maximal release and to define sensitivity to heparin-facilitated lipase release. Maximal postheparin LPLA and HTGLA (u/ml plasma or u/total plasma vol) were similar in lean and obese individuals despite a nearly three-fold increase in calculated adipose tissue mass in the obese. Since adipose tissue LPLA has been reported to increase in proportion to adipocyte size, the lack of difference in maximal postheparin LPLA was expected. There was an inverse correlation between plasma triglyceride concentration and LPLA/kg adipose tissue. These empirical observations may reflect relatively decreased heparin-releaseable (functional) LPLA in relation to adipose organ mass in obese subjects. The mechanism of this relationship has not been established.
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PMID:Postheparin plasma lipase activities in obesity: failure to increase with adipose organ enlargement. 68 71

The lipoprotein-lipase activities (LPLA) and fat cell sizes were determined in subcutaneous, adipose tissue from four different sites in a group of 17 obese women. The LPLA per gram and per cell were significantly higher in the adipose tissue from gluteal and femoral sites than in tissue from the abdominal site. The degree of obesity of the subjects, as reflected in the fat cell size, was correlated with the LPLA per cell, so that large cells contained more LPLA per cell than small cells. On the other hand, no correlation was found between the cell size and the LPLA per gram. Intra-individually, the cell weight was related also to the LPLA per gram, so that sites with large fat cells also had high concentrations of LPLA per gram. The interpretation of the results with regard to obesity and to the variation in size of fat depots in an individual is discussed.
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PMID:The lipoprotein-lipase activity of adipose tissue from different sites in obese women and relationship to cell size. 71 54

A new automated potentiometric method for the determination of colipase was developed, taking advantage of the reactivation of purified lipase, in the presence of bile salt and at pH 6.5. High-fat and high-starch diets induced an opposite regulation of lipase and amylase in the rat pancreas. At the same time, the level of colipase was not influenced by nutrition. During fasting and in alloxan diabetes, the specific activity of lipase almost doubled, that of amylase decreased sharply, and colipase was not affected in the rat pancreas. In obese-hyperglycemic mice, suffering from obesity, hyperinsulinism, and moderate diabetes, there was also no regulation of pancreatic colipase. Thus, at variance with a number of hydrolases, there was no dietary or hormonal adaptation of colipase. However, this was probably without any bearing on intraluminal lipolysis. Indeed, comparison of lipase and colipase activities in pancreas and in small intestine suggests that colipase concentration is not a limiting factor of intraluminal lipolysis. The molecular mechanism of this assumption is discussed on the basis of in vitro studies.
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PMID:Lack of adaptation of pancreatic colipase in rats and mice. 84 20

Published data have suggested that hypertriglyceridemia in obesity may result from the combination of hepatic overproduction and diminished removal of triglyceride-rich lipoproteins. Diminished catabolism might be expected if tissue lipoprotein lipase activity were decreased, a finding which has been reported in biopsies of adipose tissue from obese subjects. Abnormalities in heparin-released triglyceride lipase activity (PHLA) in obesity have not been reported, however. We have examined the possibility that methods for the measurement of PHLA might have failed to reveal such a defect because of the disproportionality between plasma volume and increasing body mass in obesity. Since it is usual to administer heparin on the basis of body weight, higher plasma heparin levels would be achieved in obese individuals. We performed standard PHLA assays in lean and obese volunteers. In the obese, heparin levels were consistently higher than in lean individuals although PHLA values were similar in both. Thus, PHLA in obesity appeared to be inappropriate for the heparin levels attained in plasma. Pharmacokinetic studies suggest that a decrease in PHLA available for release by heparin rather than heparin insensitivity underlies this phenomenon.
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PMID:Abnormal post-heparin lipolytic activity in obesity. A preliminary note. 120 Nov 46


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