Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two progestins with different androgenic activity were compared for their effects on plasma high density lipoproteins and postheparin plasma lipase activities in premenopausal women. Levonorgestrel, a nortestosterone-derived steroid with androgenic activity reduced plasma HDL cholesterol by 17% (P less than 0.05) and HDL2 cholesterol by 30% (P less than 0.05), without changing the HDL3 cholesterol concentration. At the same time the postheparin plasma hepatic lipase activity was increased by 56% (P less than 0.01) whereas the lipoprotein lipase was not changed. None of these effects was reproduced during administration of medroxyprogesterone acetate, a progestin with low androgenic activity. The results suggest, first, that the decrease of HDL cholesterol observed during treatment with progestins is related to the androgenic activity of the steroid used, and, second, that the change in HDL (HDL2) is caused by androgen-induced increase of hepatic lipase activity.
Atherosclerosis
PMID:Different effects of two progestins on plasma high density lipoprotein (HDL2) and postheparin plasma hepatic lipase activity. 646 May 9

In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
Atherosclerosis 1984 Sep
PMID:Post-heparin lipolytic activities and alterations of the chemical composition of high density lipoproteins in alcohol-induced type V hyperlipidemia. 649 35

The following conclusions and speculations can be tentatively drawn from the changes in lipoprotein composition and metabolism: (1) The presence of apo B-48 in serum VLDL and the high serum apo A-IV concentrations indicate a greater than normal contribution of alimentary remnant particles to the hypertriglyceridemia of uremic patients, (2) The presence of apo E and C in triglyceride-enriched serum LDL, together with the triglyceride enrichment of all lipoproteins, probably stems from a deficiency of lipoprotein lipase (LPL) and hepatic lipase (HL) activity, (3) The decreased ratio of serum apo C-II/C-III in VLDL is at least in part responsible for the depressed activity of LPL, (4) The accumulation of lipoprotein particles with distorted apoprotein and lipid patterns (particularly beta-VLDL with enrichment in cholesterol) could be associated with an increased atherogenesis because a recent study has demonstrated a strong association between raised serum IDL and VLDL concentrations and the degree of coronary atherosclerosis, (5) The increased apo E content of VLDL and HDL in uremic patients could particularly point to a disturbed cholesterol metabolism because such lipoproteins could interact with LDL at apo B, E receptors, (6) The decrease in serum HDL-cholesterol has been shown to be strongly associated with atheromatous vascular disease, and this could also hold for uremic patients; however, it is probable that low serum HDL-cholesterol together with a diminished capacity to form cholesterol-rich, apo E containing HDL represents a decrease in the antiatherogenic defense of the organism rather than an increased atherogenic potential [21].
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PMID:Recent advances in factors that alter lipid metabolism in chronic renal failure. 658 43

Plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic lipase (H-TGL) were studied in 7 patients with familial hyperchylomicronemia from four different families. Their first-degree relative were also studied. The patients were heterogeneous for the genetic defect; LPL activity was absent in five patients (LPL deficiency) but normal in two. However, these two did not have apo C-II, the physiological activator of LPL (C-II deficiency). There were no significant differences in the clinical picture between patients with LPL deficiency and C-II deficiency. In both mutants, marked hypertriglyceridemia was due to an accumulation of lipoproteins of density less than 1.006 g/ml. The LDL fraction was very reduced and abnormal in composition, presenting a CH/TG ratio of 0.5. The plasma apolipoprotein B (apo B) level was low (67 +/- 5.5 mg/dl) and was transported mainly in the VLDL fraction (26 +/- 3.2 mg/dl) rather than in the LDL fraction (15 +/- 1.4 mg/dl). Very low levels of cholesterol and apolipoprotein A-I in HDL subfractions HDL2 and HDL3 were also recorded. Only 3 out of the 24 first-degree relatives of patients with LPL deficiency showed even a small increase in plasma triglycerides, but 15 had low or low to normal LPL values. H-TGL levels were normal in all subjects. The 4 first-degree relatives of C-II deficiency patients showed normal levels of plasma lipids. LPL and H-TGL, and 2 children of 1 patient showed normal distribution of apo C peptides in their VLDL. A block in chylomicron catabolism, due to the absence of LPL or apo C-II, may lead to a massive accumulation of lipoproteins with a density less than 1.006 g/ml, and a drastic reduction in the LDL and HDL fractions. Low LPL values in the first-degree relatives of LPL deficiency patients might represent a biochemical marker for healthy carriers of LPL deficiency.
Atherosclerosis 1983 Oct
PMID:Familial lipoprotein lipase and apolipoprotein C-II deficiency. Lipoprotein and apoprotein analysis, adipose tissue and hepatic lipoprotein lipase levels in seven patients and their first degree relatives. 665 13

The distinct increase in the highly atherogenic plasma low-density lipoproteins (LDL) caused by the wellknown LDL-receptor defect is considered to be responsible for the development of atherosclerosis in familial hypercholesterolemia (FH). In contrast to the atherogenic LDL, the high-density lipoproteins (HDL) are considered to have a protective effect against the development of atherosclerosis and have hitherto been insufficiently investigated in association with FH. HDL2 are assumed to be important in the removal of free cholesterol from the peripheral tissue to the liver, but this hypothesis needs to be supported by further experimental investigations. In this study 18 patients (7 men/11 women) with familial hypercholesterolemia (FH) were compared with 18 healthy controls (8 men/10 women). From fasting plasma the following parameters were determined: cholesterol, triglycerides, phospholipids, HDL-cholesterol, by rate zonal ultracentrifugation the lipoproteins VLDL (very low-density lipoproteins), IDL (intermediate-density lipoproteins), LDL (low-density lipoproteins), HDL2 and HDL3, as well as the activities of lipoprotein lipase (LPL) and hepatic lipase (HTGL). In addition, the percentage composition of the major apolipoproteins (apo) of HDL2 and HDL3 were determined by polyacrylamide disc-gel electrophoresis. In LDL of patients with FH the percentage amount of protein was significantly (p less than 0.01) smaller than in controls. Furthermore, in HDL2 of patients with FH, the percentage content of apo-A II and apo-D was significantly (both p less than 0.01) higher than in controls. In HDL3 of patients with FH a significantly smaller (p less than 0.02) amount of apo-E was revealed than in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atherosclerosis in familial hypercholesteremia possibly induced by defective HDL]. 671 Jan 13

Lipoprotein lipase (LPL) is an enzyme which hydrolyses triglycerides especially VLDL and chylomicrons triglycerides. The measurement of LPL can be of interest in clinical biochemistry. There is no LPL in blood circulation, but it is possible to release it by heparin intravenous injection. However, heparin releases also other enzymes, particularly hepatic triglyceride lipase (HTGL). It is then post-heparin lipolytic activity (PHLA) which is determined. It is possible to measure separately LPL and HTGL, by using antibodies or inhibitors so chosen to be specific to one or the other enzyme. The main variations of LPL and HTGL in various diseases or treatments at present known are reported. LPL has also been recently involved in atherosclerosis pathogeny.
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PMID:[Lipoprotein lipase. Interest in clinical biochemistry (author's transl)]. 698 74

Immunochemical methods for selective measurement of lipoprotein lipase and hepatic lipase activities in rat postheparin plasma are described and validated. Lipoprotein lipase was measured using a substrate containing 10% serum and 0.1 M NaCl after inactivation of hepatic lipase with a specific antiserum. Hepatic lipase was measured at 1.0 M NaCl with a serum-free substrate. The heparin dose-response curve indicated maximum relase of both activities at a heparin dose of 500 IU/kg. The lipase activities in rat postheparin plasma were 3 to 4-fold higher than those in human postheparin plasma. The LPL activity in female rats was significantly higher than in males whereas there was no sex difference for hapatic lipase.
Atherosclerosis 1980 Apr
PMID:Immunochemical assay of rat postheparin plasma triacylglycerol lipases. 699 Sep 38

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.
Atherosclerosis 1982 Feb
PMID:Plasma high density lipoproteins HDL2, HDL3 and postheparin plasma lipases in relation to parameters of physical fitness. 706 71

The postheparin plasma lipoprotein lipase (LPL) activity and plasma HDL and LDL cholesterol concentrations, decreases significantly during probucol treatment of the rat. The reduction of the LPL activity obviously took place in adipose tissue. The activity of hepatic lipase and the in vitro synthesis of cholesterol in the liver or isolated jejunal villous cells were unaffected by the probucol treatment. Plasma triglyceride and VLDL cholesterol concentrations remained similar in the control and probucol groups despite the difference in the LPL activity, whereas the esterified VLDL cholesterol level was significantly reduced in the probucol group. The results suggest that the HDL lowering action of probucol is contributed by the reduced LPL activity probably via impaired VLDL metabolism.
Atherosclerosis
PMID:Effect of probucol on cholesterol synthesis, plasma lipoproteins and the activities of lipoprotein and hepatic lipase in the rat. 733

Previous animal studies have shown that the heparin-releasable hepatic lipase (HL) is located on the luminal surface of the liver endothelial cells and may have a function in the removal of high density lipoprotein lipids from plasma. We therefore examined the relationship between plasma HDL levels and the HL activity of postheparin plasma in a group of young, very fit men who were living under strictly controlled comparable conditions (military academy studients). HDL2 cholesterol, HDL2 phospholipid and HDL2 protein concentrations each showed a highly significant negative correlation with postheparin HL activity. A similar but slightly lower inverse relationship was also present between total HDL lipids and HL activity, whereas no correlation could be observed between any of the HDL3 lipids and HL activity. The cholesterol/protein ratio of HDL2 correlated negatively with the HL activity. These results support the hypothesis that the hepatic endothelial lipase has a physiological role in the degradation and removal of circulating HDL2.
Atherosclerosis 1980 Aug
PMID:Evidence for the role of hepatic endothelial lipase in the metabolism of plasma high density lipoprotein2 in man. 741 75


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