Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of studies has shown that the plasma levels of high density lipoprotein (HDL) are increased by regular aerobic exercise. The plasma HDL, particularly HDL2, is regulated by the activity of 2 endothelial lipases, viz. lipoprotein lipase (LPL) and hepatic lipase (HL), which both can be assayed in postheparin plasma. In the present study the plasma levels of HDL2 and HDL3 cholesterol and the postheparin plasma lipase activities were related to parameters of physical fitness obtained from a pulse conducted maximal bicycle ergometer test. There was a significant positive correlation between HDL2 cholesterol and physical fitness (r = 0.52, P less than 0.01). On the other hand, the postheparin plasma hepatic lipase activity showed a significant negative correlation to physical fitness (r = -0.57, P less than 0.01). The HDL2 cholesterol was inversely correlated with the HL activity (r = 0.57, P less than 0.001). Application of partial correlation analysis to the data showed that the relationship between HDL2 cholesterol and fitness disappeared by keeping the HL activity constant whereas the correlation between HDL2 and HL was not influenced by fitness. The relation of HDL2 to fitness was independent in body fat and basal plasma insulin level; in addition the relationship between HL and fitness was not accounted for by body fatness. No relationship was found between physical fitness and LPL activity or between HDL3 and fitness. The results support the hypothesis that hepatic endothelial lipase has a role in the regulation of plasma HDL2 cholesterol and that the activity of this enzyme decreases upon increase of physical fitness.
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PMID:Plasma high density lipoproteins HDL2, HDL3 and postheparin plasma lipases in relation to parameters of physical fitness. 706 71

The effect of lipolysis of human plasma very low density lipoproteins (VLDL) on the distribution of high density lipoprotein subfractions was studied in an in vitro system consisting of purified bovine milk lipoprotein lipase and albumin. The distribution of lipids and apoproteins (apoC-II and apoC-III) within the lipoprotein fractions corresponding to HDL2 (d = 1.063-1.120 g/ml) and HDL3 (d = 1.120-1.210 g/ml) was dependent upon the concentration of VLDL in the incubation mixture. After lipolysis of an incubation mixture containing VLDL-triglyceride (0.6 mg triglyceride/ml) and HDL3 (0.1 mg protein/ml), most of the lipid and apoproteins were recovered in HDL3. At higher concentrations of VLDL-triglyceride relative to HDL3-protein (1.8 or 2.4 mg of VLDL-triglyceride and 0.1 mg of HDL3-protein) the amount of lipid and apoprotein isolated in the HDL3 density fraction decreased after lipolysis and there was an increase in the amount isolated between d 1.063-1.120 g/ml. These results provide additional evidence for the conversion of HDL3 to HDL2 during lipolysis. Furthermore, they suggest that the relative distribution of plasma HDL2 and HDL3 is related to the rate of catabolism of triglyceride-rich lipoproteins.
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PMID:In vitro catabolism of human plasma very low density lipoproteins. Effects of VLDL concentration on the interconversion of high density lipoprotein subfractions. 706 84

The concentrations of plasma high density lipoprotein (HDL) and its subfraction HDL2 are influenced by endogenous and exogenous sex hormones. The catabolism of HDL2 is mediated by a lipolytic enzyme, hepatic lipase, which is present in endothelial cells covering the liver sinusoids. Since the activity of this enzyme is also regulated by gonadal and anabolic steroids, we examined whether the effect of sex steroids on plasma HDL is related to changes in hepatic lipase. In postmenopausal women, estradiol valerate (2 mg/day, orally) increased the HDL2 cholesterol and phospholipid concentrations by 20% (P less than 0.05). Simultaneously, the hepatic lipase activity of postheparin plasma decreased by 25% (P less than 0.05). The addition of levonorgestrel (250 micrograms/day, orally) to the treatment reversed both effects of estrogen, so that HDL2 cholesterol and phospholipid levels fell below and hepatic lipase activity rose above the respective pretreatment values. The hormones did not influence the HDL3 lipid concentrations or the lipoprotein lipase and lecithin:cholesterol acyltransferase activities. The results are compatible with the hypothesis that the effects of sex steroids on plasma HDL (HDL2) are mediated by changes in hepatic lipase activity.
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PMID:High density lipoprotein-2 and hepatic lipase: reciprocal changes produced by estrogen and norgestrel. 707 94

We investigated high density lipoprotein (HDL) subfractions in abetalipoproteinemia (ABL) using rate zonal ultracentrifugation. In ABL, HDL2 is the major subfraction, 65% of total mass compared to less than 10% in normal subjects with similar HDL levels. HDL2 and HDL3 in ABL (n = 3) are larger and lighter than in normals (n = 3), with mean diameters of 136 +/- 19 A and 100 +/- 12 A, respectively (as compared to 113 +/- 12 A and 86 +/- 11 A), and contained more apoprotein E. ABL-HDL2 and HDL3 particles contain 2- to 2.5-fold more cholesteryl ester molecules than normals. ABL-HDL can be modified towards normal HDL by allowing VLDL triglycerides to exchange for ABL-HDL cholesteryl esters, followed by addition of lipoprotein lipase and hydrolysis of the triglycerides. In addition, ABL plasma contains a previously undescribed small and spherical (61 +/- 8 A) protein-rich (63% by weight) HDL fraction, which we call ABL-HDL4. Our data suggest that absence of cholesteryl ester transfer to triglyceride-rich lipoprotein in ABL causes accumulation of abnormally large cholesteryl ester-rich particles.
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PMID:Abnormal high density lipoproteins of abetalipoproteinemia: relevance to normal HDL metabolism. 716 57

High density lipoprotein subfractions HDL2 and HDL3 were separated from plasma of 22 normolipidemic healthy human subjects and analyzed for cholesterol, triglyceride, phospholipid and protein. In the same subjects the heparin-releasable lipoprotein lipase activity was assayed from biopsies of adipose tissue and skeletal muscle. A significant inverse correlation was found between the plasma concentrations of HDL2 and HDL3 (4= -0.55, p less than 0.01). The HDL2 cholesterol and HDL2 phospholipid levels were negatively correlated with HDL3 protein levels. The total HDL2 and HDL2 cholesterol, phospholipid and protein concentrations were all positively correlated with lipoprotein lipase activity of both adipose tissue and skeletal muscle. In contrast, the corresponding HDL3 values did not show any correlation with adipose tissue lipoprotein lipase but the HDL3 cholesterol, triglyceride and protein levels were inversely correlated with skeletal muscle lipoprotein lipase activity. The results suggest that plasma HDL2 and HDL3 concentrations are reciprocally regulated by the activity of lipoprotein lipase. THe data are compatible with a concept proposing conversion of HDL3 to HDL2 through assimilation of cholesterol, phospholipids and apoproteins from triglyceride-rich lipoproteins during their degradation by lipoprotein lipase. Particularly the concentration of the HDL2 is closely related to the rat of intravascular lipolysis.
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PMID:High density lipoprotein subfractions in relation to lipoprotein lipase activity of tissues in man--evidence for reciprocal regulation of HDL2 and HDL3 levels by lipoprotein lipase. 723 31

Seventeen previously sedentary men (aged 30-45) were exercised approximately twice weekly over a 10-week period during which time there was a significant fall in low density lipoprotein cholesterol, but total high density lipoprotein (HDL) did not change. The subfraction HDL2 showed an initial fall at two weeks of training with a subsequent rise above the baseline by 10 weeks. HDL3 cholesterol tended to change in an opposite direction to HDL2 thus accounting for no significant change in total HDL cholesterol. Smoking or drinking habits did not change throughout the study. As body weights did not change significantly through the study, energy intake must have increased with probable increased very low density lipoprotein (VLDL) production. Loss of apoprotein C-peptides from HDL2 associated with activation of lipoprotein lipase, and clearance of VLDL, could have caused redistribution of C-apoproteins between HDL3 leading to the changes seen, with the establishment of a new equilibrium with continued training by 10 weeks.
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PMID:Changes in high density lipoprotein subfractions and other lipoproteins by exercise. 723 42

In order to localize the labelled apolipoproteins C removed from Very Low Density Lipoproteins (VLDL) during lipolysis by lipoprotein lipase, we used human VLDL labelled with 125I-labelled apolipoproteins C and employed density gradient ultracentrifugation to analyze lipolytic products. Triacylglycerol hydrolysis occurs when albumin is present even in the absence of serum or High Density Lipoproteins (HDL). In this case, apolipoproteins C were found to be located in several fractions, in different density regions. When either HDL or serum were present in the incubation medium, the removed apolipoproteins C were recovered in only one main fraction in the high density region (1.10 g/ml). Incubations in the presence of either HDL2 or HDL3 gave quite similar results.
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PMID:Redistribution of apolipoproteins C removed from human very low density lipoprotein during in vitro lipolysis by lipoprotein lipase. 726 Jan 73

Post-heparin lipoprotein lipase (PH-LPL)-high density lipoprotein cholesterol (HDL-C) interrrelationships were assessed in 9 subjects with documented familial hyperalphalipoproteinemia (FHA) and in 8 controls to focus on potential biochemical etiologies of FHA and relationships of HDL-C to triglyceride hydrolysis and PH-LPL. FHA subjects had mean HDL-C and HDL2-C levels > twice controls; their PH-LPL levels (mean +/- SEM) (3.14 +/- 2.3 mumol FFA/h/ml) were also > twice that of controls (15.0 +/- 1.6) (P < 0.01), but post-heparin hepatic lipase levels (PH-HL) in the FHA and control subjects did not differ (18.1 +/- 1.6 vs 26.6 +/- 4.3, P > 0.1). For all subjects (FHA and controls) PH-LPL was positively correlated with HDL-C (r = 0.79, P < 0.01) and with HDL2-C (r = 0.90, P < 0.01), but not with HDL3-C (r = --0.02). There were no significant PH-HL and HDL-C interrelationships, P > 0.1. The amount of apo CII (the primary activator of PH-LPL) in HDL2 was greater in the FHA (mean +/- SEM) (16.1 +/- 2.5 microgram/ml plasma) than in control subjects (4.7 +/- 0.9, P < 0.01). There were strong positive correlations between HDL2 apo CII and both PH-LPL (r = 0.79, P < 0.01) and HDL2-C (r = 0.80, P < 0.01). Apo CII as a percentage of HDL2 protein was higher in FHA than control subjects (mean +/- SEM) (1.2 +/- 0.3% vs 0.5 +/- 0.2%, P < 0.01). Apo CII as a percentage of HDL3 protein was similar in FHA and control subjects. We postulate that increased turnover rate of triglyceride-rich lipoproteins due to high LPL activity may be an important factor leading to the elevation of HDL-C in FHA. The highly significant positive correlation between HDL2-C and PH-LPL provides strong clinical evidence for the theory that HDL2 is formed during the hydrolysis of triglycceride-rich lipoproteins. The high concentration of HDL2 apo CII in FHA subjects may be caused by increased catabolism of triglyceride-rich lipoproteins in the presence of high endothelial LPL, with transfer of apo CII from very low to high density lipoproteins.
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PMID:Post-heparin plasma lipoprotein and hepatic lipases. Relationships to high density lipoprotein cholesterol and to apolipoprotein CII in familial hyperalphalipoproteinemic and in normal subjects. 742 98

The following studies have been carried out to compare the effects of fish protein with other dietary proteins on plasma cholesterol and lipoproteins in animal models and in humans. In rabbits, fish protein has been shown to induce relatively variable effects compared to casein and soy protein on serum cholesterol depending in part on the origin of dietary lipids with which it is combined. In a protein-lipid interaction study, casein, soy or cod protein were combined with corn or coconut oil. Casein and soy protein in the presence of corn oil induced lower serum cholesterol levels despite its combination with either corn or coconut oil. This is in part due to serum high density lipoprotein (HDL) cholesterol concentrations, which were consistently higher with cod protein than with either casein or soy protein, regardless of the dietary lipid source. In rabbits, this rise in HDL cholesterol was associated with a decrease in very low density lipoprotein (VLDL) triglycerides and an increase in postheparin plasma lipoprotein lipase activity. The effects of lean white fish on plasma lipoproteins also have been investigated in post and premenopausal women fed a low-fat, high P/S (polyunsaturated/saturated fat) ratio diet. In postmenopausal women, lean white fish compared with other animal protein products induced higher concentrations of plasma cholesterol, LDL-apolipoprotein (apo) B and HDL cholesterol, mainly in the HDL3 fraction. In premenopausal women, lean white fish induced lower concentrations of VLDL triglycerides and higher concentrations of LDL-apoB in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of dietary fish protein in the regulation of plasma lipids. 758 95

Numerous studies have reported that women have a lipoprotein profile suggestive of a reduced risk of coronary heart disease (CHD). We have therefore tested whether the "protective" lipoprotein profile of women could be explained by differences in hepatic lipase (HL) or lipoprotein lipase (LPL) activities. In the present study, 14 non-obese healthy premenopausal women had higher plasma concentrations of high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, and HDL-apolipoprotein (apo) AI, and a higher ratio of HDL-C to low-density lipoprotein cholesterol (LDL-C) than 17 non-obese healthy men. Women also had lower plasma triglyceride (TG), HDL-TG, and apo B levels than men. Plasma postheparin LPL (PH-LPL) and HL activities showed no significant sex dimorphism, whereas abdominal and femoral adipose tissue (AT)-LPL activities were significantly higher in women (P < .005). In men, PH-LPL activity correlated significantly with plasma HDL2-C (r = .52, P < .05), LDL-C (r = -.47, P < .05), and apo B (r = -.56, P < .01) levels, as well as with the HDL-C/LDL-C ratio (r = .67, P < .005). No such relationships were found in women, with the exception of HL activity, which was negatively correlated with HDL-apo AI levels. In both genders, abdominal AT-LPL activity showed no significant association with plasma lipoprotein levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does lipoprotein or hepatic lipase activity explain the protective lipoprotein profile of premenopausal women? 772 72


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