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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concern about a possible association between oral contraceptives (OCs) and cardiovascular problems has led to investigation of the effects of OC use on plasma lipids and lipoproteins. The lipoprotein metabolic system involves chylomicrons derived from dietary fat, very-low-density lipoproteins (VLDL) derived primarily from the liver, and high-density lipoproteins (HDL). VLDLs form remnantlike particles termed intermediatedensity lipoproteins (IDLs), which ultimately are converted to low-density lipoproteins (LDLs). Understanding of how these particles relate to the atherogenic process is incomplete, although the spectrum of VLDL-LDL particles is involved in atherosclerosis. Whereas the LDLs and IDLs can deliver cholesterol to the artery wall, the HDLs seem to be involved in bidirectional cholesterol transport and are capable of accepting cholesterol from tissues and other lipoprotein classes. This property has caused HDL to become known as an antiatherogenic lipoprotein. Estrogen appears to increase VLDL production rates as well as the clearance of remants and LDL, although genetic factors may be involved. Estrogen's effect on HDL seems to be a more uniform increase in production. In contrast, synthetic progestational steroids appear to reduce HDL, in part due to the increased metabolism of HDL lipids mediated by hepatic lipase activity. They appear to interact with estrogen to raise LDL and VLDL levels. Epidemiologic studies suggest that low- and high-density cholesterol provide the best clinical indices of cardiovascular risk. When the HDL level is low, coronary risk amplifies; when the HDL level is high, the LDL effect on coronary risk compresses. There is as yet no precise information on the extent to which changes in lipoproteins, especially HDL, affect the development or progression of coronary artery disease.
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PMID:Effects of oral contraceptives on lipid metabolism. 372 87

Oligosaccharide fragments of heparin were prepared using flavobacterial heparinase. Following sizing, these oligosaccharide fractions were administered (i.v.) to rabbits and were examined for their ability to release lipoprotein lipase. The decasaccharides (dp = 10, Mr avg = 2,800) were the smallest oligosaccharides which resulted in substantial lipase release. The plasma lipase levels obtained with decasaccharides were comparable to low molecular weight heparin and one-third those obtained when heparin was administered at an equivalent dose. The peak plasma lipase concentration was observed 10 min following heparinization and fell off rapidly over the 60-min time course. The lipase release activity paralleled the in vivo pharmacokinetics of the heparin and decasaccharide sample as determined by monitoring their anti-Factor Xa activity. No activation of purified bovine milk lipoprotein lipase or plasma lipase was detectable at the concentrations studied, indicating that the increase in circulating lipolytic activity was due entirely to release. Lipoprotein lipase accounted for a major portion of the released activity with hepatic triglyceride lipase representing the remainder of the lipolytic activity. The sized decasaccharide sample was characterized with regards to its structure and anticoagulant activity. The decasaccharides exhibited reduced anticoagulant activity possibly making it a better drug candidate in the treatment of atherosclerosis.
Atherosclerosis 1986 Nov
PMID:Effect of very low molecular weight heparin-derived oligosaccharides on lipoprotein lipase release in rabbits. 380 Oct 83

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

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.
Atherosclerosis 1985 Apr
PMID:A comparative study of the effects of acipimox and clofibrate in type III and type IV hyperlipoproteinemia. 392 65

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.
Atherosclerosis 1986 Feb
PMID:Rapid decrease in high density lipoprotein subfractions and postheparin plasma lipase activities after cessation of chronic alcohol intake. 396 41

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.
Atherosclerosis 1985 Apr
PMID:The effect of etophylline clofibrate on HDL subfractions. 400 84

Selective inhibition of hepatic triglyceride lipase (HTGL) by specific antibodies in rats led to an altered VLDL apoprotein composition. Apoprotein analysis by isoelectric focusing revealed a new protein band in VLDL and an increase in apoprotein E (apo E) content. Apoproteins in LDL and HDL remained unchanged. Electronmicroscopy showed a significant increase in particle size of VLDL from 452 to 497 A with no significant changes in LDL and HDL diameters.
Atherosclerosis 1984 Dec
PMID:Plasma apoprotein changes after selective inhibition of hepatic triglyceride lipase in rat. 608 98

In an attempt to define the role of hepatic triglyceride lipase in plasma lipoprotein metabolism, in vivo experiments using an antibody specifically prepared against this enzyme were conducted in rats. The antibody gamma globulins were injected into rats three times during a 40 min period. Control rats received non-immune rabbit gamma globulins prepared in the same way as the immune gamma globulins. After treatment, blood was taken and the plasma was separated. Plasma lipoproteins were fractionated by ultracentrifugation into VLDL, IDL, LDL and HDL. Treatment of recipient rats with the antibody significantly increased cholesterol, phospholipid and protein concentrations in the IDL fraction. These concentrations were also elevated in the LDL fraction. However, we speculate that this increase represents the accumulation of small remnants rather than bona fide LDL. VLDL compositions in antibody-treated rats did not differ from those in control animals. In HDL, only the phospholipid level was elevated in antibody-treated rats. The data of the present study indicate that hepatic triglyceride lipase mediates the catabolism of remnant lipoproteins by the liver.
Atherosclerosis 1981 Jun
PMID:Accumulation of intermediate density lipoprotein in plasma after intravenous administration of hepatic triglyceride lipase antibody in rats. 616 74

Post-heparin lipase activities were measured in normolipemic men with complaints suggestive of symptomatic coronary artery disease. A study group, who showed diffuse atherosclerotic narrowing of the coronary vessels, assessed by a quantitative computer-assisted analysis method, had a lowered hepatic lipase in comparison with a group with normal angiograms. Lipoprotein lipase was lower in the study group but well within the normal range and not statistically different. Some related hormones (cortisol, estradiol, testosterone and glucagon) were different in the two groups while others (insulin, human growth hormone, prolactin, thyroid hormones) were not. The results are discussed in view of the proposed role of hepatic lipase in the uptake of HDL-cholesterol by the liver.
Atherosclerosis 1983 Sep
PMID:Post-heparin lipases, lipids and related hormones in men undergoing coronary arteriography to assess atherosclerosis. 635 16

We examined possible determinants of serum high density lipoprotein cholesterol (HDL-C) concentrations in 56 male distance runners (aged 20-56 years) by comparing runners whose HDL-C were either above or below the group median of 63 +/- 13 (+/- SD) mg/dl. HDL-C averaged 53 +/- 7 mg/dl for runners below and 73 +/- 11 mg/dl for runners above the median. Neither exercise training (miles run per week, years of running), physical characteristics (height, weight, adiposity), or dietary factors (total daily caloric intake and daily caloric intake from protein, fat, saturated fat, polyunsaturated fat, carbohydrate, and alcohol) differed between the two groups (P greater than 0.05, MANOVA). Apo A-I (P less than 0.01) was higher and triglyceride concentrations lower (P = 0.07) in the high HDL-C group. The data were also analyzed by comparing runners in the lowest and highest tertiles for HDL-C values and essentially the same results were obtained. When all runners were combined, neither training, physical characteristics nor dietary intake was significantly related to HDL-C (P greater than 0.05). Total cholesterol and apo A-I were directly related (r = 0.35 and r = 0.66, respectively, P less than 0.01) and triglycerides inversely related (r = -0.31, P less than 0.05) to HDL-C. Plasma post-heparin lipoprotein lipase activity (LPLA), hepatic triglyceride lipase activity (HTGLA), and HDL-C subfractions were measured in 22 runners.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1984 Dec
PMID:Training, diet and physical characteristics of distance runners with low or high concentrations of high density lipoprotein cholesterol. 644 53


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