Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We sought to determine the optimal dose of heparin for evaluating the activities of lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase (HTGLA) in postheparin plasma. Nine physically active and ten sedentary men (age 30 +/- 5 yr, mean +/- SD) received 30, 50, 75, and 100 IU/kg of heparin in random order during a 2-week period. Based on all the samples, the average LPLA in the athletes was 43% higher (P less than 0.001) and HTGLA was 19% lower than in the untrained subjects (NS). The greatest LPLA was obtained after a heparin dose of 75 IU/kg, but LPLA after the three highest doses were not significantly different. There was also a dose effect on HTGLA (P less than 0.001) with greatest activities following doses of 75 and 100 IU/kg. Despite these dose effects, subjects maintained their rank order for both postheparin lipase activities regardless of the heparin dose. The only exception was for LPLA in the sedentary men probably because of lower LPLA and a smaller range of values. We also examined the effect of repeated daily injections of 75 IU/kg heparin on LPLA, HTGLA, and serum lipids. Repeated heparin administration on three consecutive days produced no significant effects on the apparent lipase activities. When all subjects were combined, HDL-cholesterol was increased over time (P less than 0.05) due to increases in both the HDL2 (P less than 0.05) and HDL3-cholesterol (NS) subfractions. Infusion of heparin or saline on three consecutive days into 18 additional men, however, had no effect on any lipid parameter.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Postheparin plasma lipolytic activities in physically active and sedentary men after varying and repeated doses of intravenous heparin. 377 28

We studied the effects of a single exercise session on lipid and lipoprotein concentrations and on postheparin plasma lipoprotein lipase (LPLA) and hepatic triglyceride hydrolase activities (HTGLA) in 11 trained (T) and ten untrained (UT) men. Subjects exercised on a bicycle ergometer at 80% of their maximal heart rate for one (UT) or two hours (T). Blood samples were drawn 24 hours before and at ten minutes and 24, 48, and 72 hours after exercise. Values were analyzed before and after adjustment for estimated changes in plasma volume (PV). High density lipoprotein cholesterol (HDL-C) increased 2 +/- 4 mg/dL in T (P less than 0.05) and 1 +/- 2 mg/dL in UT subjects beginning 48 hours after exercise. This increase was magnified by adjusting for the 5% to 8% postexercise expansion of PV. The increase in HDL in the T subjects was produced by increases in the HDL2-C subfraction (+3 +/- 4 mg/dL, P less than 0.05) whereas HDL3 increased in the UT men (+2 +/- 3 mg/dL, P less than 0.05). LPLA did not change in either subject group when estimated PV changes were ignored but increased 11% (P less than 0.05) at 24 hours after exercise when PV was considered. HTGLA was 11% below baseline in the UT men 24 to 72 hours after exercise (P less than 0.05) but showed no change in either subject group after adjustment for PV. These results demonstrate that exercise acutely increases HDL levels by raising the HDL2 subfraction in T and the HDL3 subfraction in UT men.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Exercise acutely increases high density lipoprotein-cholesterol and lipoprotein lipase activity in trained and untrained men. 380 90

Acipimox, an analogue of nicotinic acid, is a hypolipidemic drug with antilipolytic activity. Ten patients with type III and 10 with type IV hyperlipoproteinemia participated in a comparative open cross-over study of the effect of acipimox (750 mg/day) and clofibrate (2 g/day) on lipoproteins, apoliproproteins and postheparin lipase activities during 6 weeks. During acipimox treatment 2 type III patients complained of flushing, resulting in one drop-out. In the type III patients serum cholesterol decreased 30% (P less than 0.01) during treatment with acipimox and 24% (P less than 0.01) with clofibrate, and serum triglycerides 48% (P less than 0.01) and 34% (P less than 0.01), respectively. In the type IV patients serum cholesterol remained unchanged and serum triglycerides decreased 34% (P less than 0.05) and 35% (P less than 0.01), respectively. HDL cholesterol increased during treatment with both drugs in both groups between 6 and 15% (P less than 0.05) mainly due to a rise in HDL3 cholesterol (d greater than 1.100 g/ml). LDL cholesterol increased significantly during treatment with clofibrate, but not with acipimox. There were no or slight changes in the apoproteins A and B. Postheparin lipoprotein lipase increased during clofibrate treatment and hepatic lipase decreased during acipimox treatment. We concluded that acipimox in a dose of 750 mg/day has a similar hypolipidemic effect as 2 g clofibrate daily in type III and IV hyperlipoproteinemia.
 ...
PMID:A comparative study of the effects of acipimox and clofibrate in type III and type IV hyperlipoproteinemia. 392 65

Cholesterol esters accumulating in human plasma high density lipoproteins (HDL) are important in conversion of HDL3 to larger HDL2. We studied whether mechanisms of removal of cholesterol esters from HDL might be important in a reverse direction, i.e. conversion of HDL2 to HDL3. Native HDL2 or HDL3 is incubated with very low density lipoproteins (VLDL) and lipoprotein-poor plasma (d greater than 1.21 g/ml) at 37 degrees C. After incubation, "modified" (M) VLDL, and HDL2 or HDL3 are reisolated by ultracentrifugation. In modified M-HDL2 or M-HDL3, triglyceride becomes the major core lipid as the triglyceride/cholesterol ester weight ratio increases 8-10-fold relative to native HDL. With only small changes in protein/phospholipid ratios in M-HDLs, the large decrease in cholesterol ester/protein ratios suggest net cholesterol ester loss from HDL. Quantitative recovery analyses prove that the cholesterol esters lost from HDL are transferred to M-VLDL, which is now richer in cholesterol ester and poorer in triglyceride. These substantial exchanges of HDL lipids are not associated by significant transfer of HDL apoproteins but are dependent on neutral lipid transfer factors present in human lipoprotein-poor plasma (d greater than 1.21 g/ml). Similar results are obtained when purified core lipid transfer protein replaces d greater than 1.21 g/ml plasma in these incubations. After depletion of cholesterol ester from HDL, most but not all, exchanged triglyceride can be removed by lipolysis with either hepatic or lipoprotein lipase, resulting in a post-lipolysis HDL2 with an increased triglyceride content relative to normal HDL. With successive incubations with VLDL, and core lipid transfer factors, HDL2 loses more than two-thirds of its cholesterol esters. After lipolysis of acquired triglyceride, HDL2 is remodeled, in both composition and flotation parameters, toward HDL3.
 ...
PMID:Conversion of human plasma high density lipoprotein-2 to high density lipoprotein-3. Roles of neutral lipid exchange and triglyceride lipases. 395 20

Regular intake of alcohol is associated with elevated levels of high density lipoproteins (HDL). Opinions differ, however, on the HDL subfraction which is preferentially influenced by alcohol. In the present study we measured the HDL subfraction lipid and protein concentrations and postheparin plasma lipase activities in chronic alcohol users immediately after cessation of drinking and sequentially during one week of total abstention. The HDL2 mass concentration decreased significantly already during two abstinent days the decline continuing until the 8th day. At this time the mean HDL2 concentration had decreased by 38% from the initial value (P less than 0.05). The HDL2 cholesterol, phospholipid and protein concentrations decreased in approximately similar proportions, whereas the HDL2 triglyceride increased by 40%. The HDL3 mass concentration decreased by 13% but this change was not significant. Also in HDL3 the cholesterol, phospholipid and protein contents decreased to a similar extent but the triglyceride content rose. The postheparin plasma lipoprotein lipase activity decreased by 41% and the hepatic lipase by 37% during the abstention. It is concluded that in chronic alcoholics HDL2 accounts for the major part of the increase in HDL.
 ...
PMID:Rapid decrease in high density lipoprotein subfractions and postheparin plasma lipase activities after cessation of chronic alcohol intake. 396 41

The sequence of alterations in the concentration and composition of different plasma lipoproteins following alcohol intake is not known. We therefore monitored the concentrations of cholesterol, triglycerides, phospholipids, and proteins in the major lipoprotein fractions (VLDL, LDL, HDL2, and HDL3) in ten nonalcoholic healthy male volunteers who were given 5.5 g of alcohol per kilogram of body weight during 21/2 days (a weekend). In addition, lipoprotein lipase activity was measured in post-heparin plasma and in adipose tissue and hepatic lipase activity was measured in post-heparin plasma before and after the experiment. in a separate control experiment, the same subjects received meals and liquids without alcohol. Blood alcohol levels remained below 1.5 g/L. Alcohol caused a progressive increase in the fasting VLDL triglyceride and phospholipid concentrations, both of which were doubled during the experiment (P less than 0.001). In contrast, the VLDL cholesterol levels remained unchanged until the third morning, when there was a slight increase. The LDL triglyceride and phospholipid concentrations also rose without simultaneous changes in the LDL cholesterol concentration. Consistent with these changes, the HDL cholesterol concentration showed no response to alcohol during the experiment, but the HDL phospholipid level rose from 76 to 99 mg/dL (P less than 0.001). This was reflected as an increase in the HDL2 concentration from 124 to 158 mg/dL (P less than 0.01), whereas no change occurred in the HDL3 level. The increment of HDL2 concentration was due to a rise of its triglycerides, phospholipids, and apoproteins A-I and A-II but not to a rise of cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Sequence of alcohol-induced initial changes in plasma lipoproteins (VLDL and HDL) and lipolytic enzymes in humans. 396 13

The effect of lipid transfers on the structure and composition of high density lipoproteins (HDL) has been studied in vitro in incubations that contained the lipoprotein-free fraction of human plasma as a source of lipid transfer protein. These incubations did not contain lecithin:cholesterol acyltransferase activity and were not supplemented with lipoprotein lipase. Incubations were performed at 37 degrees C for 6 hr in both the presence and absence of either added very low density lipoproteins (VLDL) or the artificial triglyceride emulsion, Intralipid. Incubation in the absence of added VLDL or Intralipid had little or no effect on the HDL. By contrast, incubation in the presence of either VLDL or Intralipid resulted in marked changes in the HDL. The effect of incubation with VLDL was qualitatively similar to that of Intralipid; both resulted in obvious transfers of lipid and changes in the density, particle size, and composition of HDL. Incubation of the plasma fraction of density 1.006-1.21 g/ml, total HDL, or HDL3 with either VLDL or Intralipid resulted in the following: 1) a depletion of the cholesteryl ester and free cholesterol content and an increase in the triglyceride content of both HDL2 and HDL3; 2) a decrease in density and an increase in particle size of the HDL3 to form a population of HDL2-like particles; and 3) the formation of a discrete population of very small lipoproteins with a density greater than that of the parent HDL3. The newly formed lipoproteins had a mean particle radius of 3.7-3.8 nm and consisted mainly of protein, predominantly apolipoprotein A-I and phospholipid.
 ...
PMID:Role of lipid transfers in the formation of a subpopulation of small high density lipoproteins. 398 81

We examined the effects of lecithin:cholesterol acyl transferase (LCAT) and of lipoprotein lipase (LPL) on the conversion of high density lipoproteins (HDL) towards fractions of lower densities using the analytical ultracentrifuge. Freshly isolated whole plasma was incubated for 24 h at 37 degrees C in the presence or absence of active enzyme systems. In some cases, lipoproteins were removed by selective precipitations; alternatively, we added triglyceride-rich lipoproteins (TGRLP) or Intralipid to the incubations. The results are as follows. 1) The incubation of whole plasma containing active LCAT leads to a conversion of HDL3 to a fraction of lower density, notably HDL2a. If LCAT is inhibited, the conversion is far less pronounced. 2) If very low and low density lipoproteins are removed by phosphotungstate precipitation and the supernatant is incubated with LCAT, HDL3 shifts towards higher densities. 3) The presence of phosphatidylcholine/cholesterol liposomes or the presence of blood cells as a source of additional LCAT substrate had only little influence on the HDL conversion in our system. 4) The addition of TGRLP or of Intralipid at minimal ratios of 2.5:1 caused an almost complete conversion of HDL3 to HDL2b. This conversion was dependent on active LCAT. 5) LPL also caused a shift of HDL3 to HDL2a if TGRLP was present. HDL2b, however, was not formed by LPL unless LCAT was active.
 ...
PMID:The in vitro formation of HDL2 during the action of LCAT: the role of triglyceride-rich lipoproteins. 398 87

The effect of etophylline clofibrate on lipids and apolipoproteins of the high density lipoprotein (HDL) subfractions HDL2 and HDL3 as well as on very low density (VLDL) and low density lipoproteins (LDL) and the post heparin lipolytic activities (PHLA) of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) has been studied in 14 patients with type II hyperlipoproteinemia (HLP). The study was preceded by a 4-week washout phase, followed by a 6-week placebo period. During the next 12 weeks, the patients received 750 mg etophylline clofibrate per day. Then the drug was again replaced by placebo for another 6 weeks. During the study the patients were on a low fat diet poor in cholesterol with a P/S ratio over 1.0. HDL cholesterol and apoproteins increased significantly during treatment. In the first verum phase this effect was related to the rise in HDL2 components with minor changes in HDL3 concentrations, whereas in the second verum period a distinct increase of the HDL3 components could be detected. This development was accompanied by a significant increase of the LPL activities during the first 6 weeks of treatment, followed by a decrease to initially measured values after 12 weeks. The drug lowered plasma- and LDL-cholesterol levels by 19% and 22%, and plasma and VLDL triglycerides by 22% and 25%, respectively. VLDL-C apoproteins (C-I, C-II, C-III) declined by 31% with a percentage increase of apo C-II compared with apo C-I and apo C-III.
 ...
PMID:The effect of etophylline clofibrate on HDL subfractions. 400 84

The conversion of pig high-density lipoproteins (HDL) (mainly HDL3) to fractions of lower densities was studied by incubating pig plasma for 24 h at 37 degrees C in the presence and absence of lipoprotein lipase from bovine milk, lecithin:cholesterol acyltransferase, cholesteryl ester transfer protein and triacylglycerol-rich particles (very-low-density lipoproteins (VLDL) or Intralipid). The results can be summarized as follows. In the presence of lipoprotein lipase and at a VLDL/HDL mass ratio of 2, the F-1.210 of pig HDL was shifted from 3.3 to 4.2, which is characteristic for human HDL2. This shift was caused by the excessive increase in the free fatty acid content in HDL. If 50 g/l of bovine serum albumin were added prior to incubation, the flotation rate of HDL remained in the HDL2a region. If lecithin:cholesterol acyltransferase was active in fasting pig plasma during incubation, we observed only a negligible increase of F-1.210 in HDL. If pig lipoproteins were incubated with human lipoprotein-free serum as a source of cholesteryl ester transfer activity, a slight increase in the flotation rate of HDL was observed, which was amplified in the presence of active lecithin:cholesterol acyltransferase. Pig HDL was converted to a fraction with F-1.210 of 4.2, which is typical for human HDL2, only if active lecithin:cholesterol acyltransferase, cholesteryl ester transfer protein and triacylglycerol-rich particles were present in the incubation mixture. From our results we also concluded that apolipoprotein A-II plays no role in the HDL2 formation.
 ...
PMID:Factors affecting the conversion of high-density lipoproteins: experiments with pig and human plasma. 400 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>