Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein lipase is a key enzyme of lipid metabolism that acts to hydrolyze triglycerides, providing free fatty acids for cells and affecting the maturation of circulating lipoproteins. It has been proposed that the enzyme plays a role in the development of obesity and atherosclerosis. The human enzyme has been difficult to purify and its protein sequence was heretofore undetermined. A complementary DNA for human lipoprotein lipase that codes for a mature protein of 448 amino acids has now been cloned and sequenced. Analysis of the sequence indicates that human lipoprotein lipase, hepatic lipase, and pancreatic lipase are members of a gene family. Two distinct species of lipoprotein lipase messenger RNA that arise from alternative sites of 3'-terminal polyadenylation were detected in several different tissues.
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PMID:Human lipoprotein lipase complementary DNA sequence. 382 7

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

To define the effects of moderate alcohol intake on cholesterol and triglyceride metabolism in man, twelve patients were hospitalized on a metabolic ward and were fed defined diets for 10 weeks. Each patient underwent testing of plasma lipid and lipoprotein levels, of cholesterol metabolism (absorption, fecal excretion, bile saturation), and of triglyceride metabolism [turnover of triglycerides in chylomicrons and very low density lipoproteins (VLDL)]. This testing was done twice, first during a 4-week control period and then during a 4-week period in which 630 calories of alcohol were either added to or substituted for baseline calories. This increased the average baseline caloric intake by only 24% (range 20% to 30% depending on the initial caloric intake). Addition of alcohol to the baseline diet did not cause weight gain in lean individuals. Obese individuals' responses were more variable, and 3/6 definitely gained weight when the diet was supplemented with alcohol. In addition, obese subjects appeared to be more susceptible to the hyperlipidemic effects of alcohol; whereas 4/6 obese patients developed increased total triglyceride and VLDL-triglyceride concentrations when alcohol was administered, concentrations increased with alcohol administration in only 1/6 lean individuals. High density lipoprotein (HDL) cholesterol increased in all volunteers. Low density lipoprotein (LDL) levels did not change. Metabolic studies showed increased transport of VLDL-triglycerides in overweight patients but not in normal weight individuals; increased transport of VLDL-triglycerides in the former was associated with delayed clearance of chylomicron triglycerides. Alcohol consumption did not affect lipoprotein lipase or hepatic triglyceride lipase in six patients in whom these enzyme activities were measured. In the amounts of alcohol taken in this study, no changes were observed in absorption, synthesis, or excretion of bile acids, or percent saturation of gallbladder bile with cholesterol.
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PMID:Effects of alcohol on plasma lipoproteins and cholesterol and triglyceride metabolism in man. 673 83

Postheparin plasma-lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were investigated in rats 1 week after ventromedial-hypothalamic lesions. The enzyme activities were measured using radio-labelled triolein as a substrate. Two lipases were measured separately using specific antiserum prepared against H-TGL. VMH-lesioned rats fed ad lib. showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was a positive correlation between plasma-LPL activity and insulin levels in VMH-lesioned rats. When rats were examined after overnight fast, VMH-lesioned rats again showed an increase in plasma LPL with normal H-TGL activity and an elevation of plasma insulin. There was also a positive correlation between plasma LPL activity and insulin levels. In order to examine the effect of insulin, rats were treated with daily doses of 3 units of insulin for 1 week. Rats fed ad lib. were insulin treatment showed an increase in plasma LPL with normal H-TGL activity. These results indicate that hyperinsulinemia which was produced by VMH lesions may increase postheparin plasma-LPL activity. We speculate that this increase in plasma-LPL activity mainly reflects that of adipose tissue. The increase of LPL activity can accelerate fat deposition into adipose tissue, contributing to one of the factors causing hypothalamic obesity.
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PMID:Increase of postheparin plasma-lipoprotein-lipase activity in ventromedial-hypothalamic obesity in rats. 674 14

The relationship between obesity and alterations in adipose tissue metabolism and lipid transport was studied in fourteen obese subjects before and after a weight reduction of 4-22 kg. Blood glucose and plasma insulin patterns after peroral glucose intake improved significantly, and plasma glucagon levels decreased markedly after treatment. Plasma triglyceride and total cholesterol levels were not altered, but there was a 20% (P less than 0.05) increase in HDL concentrations. Plasma free fatty acid and glycerol concentrations decreased, in parallel to a decrease in lipolysis rate in vitro. Lipoprotein lipase and hepatic lipase activities in postheparin plasma, as well as the intravenous fat tolerance test, were normal and did not change significantly after weight loss. Lipoprotein lipase activity in adipose tissue, expressed per cell, was elevated and did not change after weight reduction. Also, the enzyme activity did not increase after glucose intake before or after treatment. The lack of effect on lipoprotein lipase activity and regulation in combination with significant improvements of other aspects of lipid and glucose transport is consistent with the view that alterations in LPL activity and regulation may represent an early and possibly primary defect in the development of obesity.
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PMID:Effects of weight reduction on plasma lipoproteins and adipose tissue metabolism in obese subjects. 680 Aug 25

Adipose tissue and muscle lipoprotein lipase and postheparin hepatic and lipoprotein lipase activities have been measured in a group of 21 Pima Indian males over a wide range of body weight to determine the relationship between obesity and these lipase activities. There was a significant positive correlation between adipose tissue lipoprotein lipase and obesity; muscle and postheparin lipoprotein lipase and hepatic lipase were not related to degree of obesity. Fasting insulin levels were not related to any of the measurements of lipase activity. There were racial differences in adipose and postheparin lipoprotein lipase activities; both were significantly lower in the Pimas as compared with a group of weight-matched Caucasian males. Lipase activities were remeasured in eight subjects after a period of weight reduction including several weeks of stabilization at the reduced weights. After the period of weight reduction adipose tissue lipoprotein lipase declined in all subjects. Hepatic lipase also declined in all but two patients. Muscle and postheparin lipolytic activities were not affected by weight loss. The data indicate that (a) there are racial differences in adipose tissue lipoprotein lipase; and (b) the elevated adipose lipoprotein lipase associated with obesity, like many other biochemical variables in the obese state, returns toward normal after weight reduction.
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PMID:Characterization of lipase activities in obese Pima indians. Decreases with weight reduction. 711 15

We previously described a new mouse model for multigenic obesity, designated BSB. We now report the use of a complete linkage map approach to identify loci contributing to body fat and other traits associated with obesity in this model. Four loci exhibiting linkage with body fat, or with the weights of four different fat depots, residing on mouse chromosomes 6, 7, 12, and 15, were identified and confirmed by analysis of additional BSB mice. Each of the four loci differed with respect to their effects on the percent of body fat, specific fat depots and plasma lipoproteins. The loci exhibited allele-specific, non-additive interactions. A locus for hepatic lipase activity was co-incident with the body fat and total cholesterol loci on chromosome 7, providing a possible mechanism linking plasma lipoproteins and obesity. The chromosome 7 locus affecting body fat, total cholesterol and hepatic lipase activity was isolated in congenic strains whose donor strain regions overlap with the chromosome 7 BSB locus. These results provide candidate genes and candidate loci for the analysis of human obesity.
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PMID:Identification of four chromosomal loci determining obesity in a multifactorial mouse model. 770 60

A radiochemical method for selective measurement of postheparin lipase activities was adapted to analyze lipoprotein lipase and hepatic lipase in preheparin plasma. The assay sensitivity was increased about four-fold by doubling both the volume of plasma used and the volume of lipolytic products taken for liquid scintillation counting, and was further improved by increasing the incubation period by 50% to 90 min. Rabbit antiserum to human hepatic lipase was unsuitable for the selective measurement of lipoprotein lipase because of apparent endogenous lipolytic activity. Preheparin hepatic lipase, however, was sensitive to inactivation by sodium dodecyl sulfate (SDS), the inhibition being greatest (> 90%) for plasma incubated with an equal volume of 40 mmol/L SDS. Intra- and interassay CVs for the two enzymes were 12.5-14.6% and 17.4-19.7%, respectively. In a cross-sectional study of 84 healthy subjects, pre- and postheparin hepatic lipase activities were higher in men than women, were correlated with indices of obesity, and were significantly correlated with one another, which explained the association of the former with plasma concentrations of high-density lipoprotein (HDL), HDL2, and small, dense low-density lipoproteins. There was no significant relationship between pre- and postheparin lipoprotein lipase activities, but the former were correlated with plasma concentrations of free fatty acids (FFA) and very-low-density lipoprotein. Apparently, preheparin activities of hepatic lipase, but not of lipoprotein lipase, may be a useful measure of the physiological function of "whole body" enzyme activity in cross-sectional and metabolic studies, where heparinization is not possible. Preheparin lipoprotein lipase activities, however, may reflect displacement of the enzyme by FFA and subsequent binding to remnants of triglyceride-rich lipoproteins.
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PMID:Measurement and physiological significance of lipoprotein and hepatic lipase activities in preheparin plasma. 788 16

The present study examined plasma lipoprotein, lipoprotein lipase, hepatic lipase, and insulin levels in men with borderline hypertension (diastolic blood pressure 85 to 94 mm Hg) compared with age-matched normotensive control subjects (diastolic blood pressure less than or equal to 80 mm Hg, n = 75 + 75). High-density lipoprotein (HDL) subclasses were determined in a subset (n = 45 + 45). While total and low-density lipoprotein cholesterol levels were similar, levels of very-low-density lipoprotein (VLDL) cholesterol and triglycerides (0.46 versus 0.41 mmol/L, P = .027, and 1.0 versus 0.85 mmol/L, P = .031) and total triglycerides (1.53 versus 1.33 mmol/L, P = .009) were elevated and HDL cholesterol was reduced in the borderline group compared with the normotensive group (1.17 versus 1.26 mmol/L, P = .043). The HDL subclass HDL2b concentration was lower (0.16 versus 0.24 mmol/L, P = .006), while HDL3b and HDL3c concentrations were higher in the borderline group (0.38 versus 0.32 mmol/L, P = .016, and 0.19 versus 0.16 mmol/L, P = .042). Significantly higher activities of hepatic lipase in the borderline group (282 versus 232 mU/mL, P = .024) and significant correlations between lipoprotein lipase activity and VLDL and HDL concentrations suggest an involvement of these enzymes in the development of these differences. When adjusted for body mass index or insulin level, all differences disappeared, except for HDL3b and HDL3c concentrations, which remained significantly elevated. These results indicate that dyslipoproteinemic changes are present in early hypertension. Although most of these changes are related to obesity, alterations in HDL profile were not explained by influences of body mass index and insulin.
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PMID:Dyslipoproteinemic changes in borderline hypertension. 796 21

It is well known that obesity is frequently associated with low levels of serum high-density lipoprotein (HDL) cholesterol. However, the mechanism for this reduction has not been fully clarified. Cholesteryl ester transfer protein (CETP) transfers cholesteryl ester from HDL to apolipoprotein B-containing lipoproteins and plays an important role in regulating the concentration and composition of HDL. To elucidate the mechanism for the reduction of serum HDL cholesterol in obesity, we analyzed serum lipoproteins, CETP, and postheparin lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities in 30 obese subjects (17 women and 13 men, age 44 +/- 14 years, mean +/- SD). We also investigated the relationship between these variables, total adiposity, and indices of body fat distribution. The average body mass index of the obese subjects was 33.1 +/- 4.8 kg/m2 (range, 26.4 to 43.8 kg/m2). The obese subjects showed significantly lower serum HDL cholesterol levels than control subjects (1.04 +/- 0.28 versus 1.50 +/- 0.34 mmol/L, P < .01). In the obese subjects, both activities and protein mass of CETP and postheparin HTGL activities were significantly increased, whereas postheparin LPL activities were significantly decreased. CETP activities, independent of postheparin HTGL and LPL activities, were correlated negatively with HDL cholesterol (r = -.39, P < .05) and the cholesteryl ester to triglyceride ratio of HDL2 and HDL3 (r = -.36, P < .05; r = -.46, P < .05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased plasma cholesteryl ester transfer protein in obese subjects. A possible mechanism for the reduction of serum HDL cholesterol levels in obesity. 801 69


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