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

Feline serum lipoproteins were fractionated into four distinct classes by density gradient ultracentrifugation and characterized with respect to physical and chemical properties. The distribution of serum lipids, lipoproteins and apolipoproteins was quite unlike that in man, the cat having five times as much high density lipoproteins (HDL) as low density lipoproteins (LDL). The lipoproteins in the d less than 1.019 g/ml fraction of cats were larger and were richer in triglycerides than their human counterparts and contained a considerable amount of beta-migrating particles. The low density lipoproteins of cats and man had similar chemical composition, but cat LDL had a higher negative charge, were smaller and contained apoprotein A-I. Cat HDL consisted of two distinct subfractions HDL2 and HDL3 with similar density boundaries and particle size as in man. In cat serum and HDL fraction apoprotein A-II was a minor component. Like human serum, fasting cat serum contained only the larger species of apoprotein B, apo B-100, whereas intestinal lymph contained exclusively the smaller apo B-48. Post heparin feline and human plasma possessed both lipoprotein lipase and hepatic lipase. Chylomicrons formed after a fat load in cats were removed from the circulation as rapidly as in man. It is concluded, that the cat is another animal model of potential interest for the study of lipoprotein metabolism.
Atherosclerosis 1987 Jul
PMID:A study of the lipid transport system in the cat, Felix domesticus. 363 43

The effect of feeding fish oil (Menhaden) on the progression of rhesus monkey atherosclerosis was determined by feeding diets containing 2% cholesterol and either 25% coconut oil (Group I), 25% fish oil/coconut oil (1:1) (Group II), or 25% fish oil/coconut oil (3:1) (Group III) for 12 months (n = 8/group). The average serum cholesterol levels were 875 mg/dl for Group I, 463 mg/dl for Group II, and 405 mg/dl for Group III. HDL cholesterol levels were 49 mg/dl for Group I, 29 mg/dl for Group II, and 20 mg/dl for Group III. An average of 79% of the aortic intima was involved with atherosclerosis in Group I, 48% in Group II, and 36% in Group III. The aortas of both fish-oil groups (II or III) contained significantly less cholesterol (total, free, and esterified), as well as less acid lipase, cholesteryl esterase, and ACAT activities when compared to the coconut-oil group (I) (p less than 0.05). Microscopically, the aortic and carotid artery lesions were smaller in cross-sectional area and in thickness, and contained less macrophages in the fish-oil groups (II and III) when compared to the coconut-oil group (I) (p less than 0.05). This protective effect was not consistently enhanced by increasing the proportion of fish oil to 3:1 (Group III) over 1:1 (Group II). The results indicate that fish oil-containing diets reduce serum cholesterol levels and inhibit atherosclerosis even in the face of lowered HDL cholesterol levels when compared to a pure coconut oil/cholesterol diet in rhesus monkeys. Therefore, fish-oil diets exert effective protective control of progression of atherosclerosis during severe atherogenic stimuli.
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PMID:Fish oil inhibits development of atherosclerosis in rhesus monkeys. 367 3

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

Lysosomal acid lipase activity was measured in mononuclear leukocytes of patients selected on the basis of premature cardiovascular disease, with or without hyperlipidemia. Enzyme activity was significantly lower in the patient population (4.8 +/- 1.3 nmol/min/mg protein, n = 190 males) than in an age-matched control population (5.4 +/- 1.3 nmol/min/mg protein, n = 124 males). There was no effect of hypercholesterolemia or hypertriglyceridemia on the enzyme activity. In the group of patients with normal plasma lipids (n = 77), 18% had mononuclear leukocyte acid lipase activity which fell below the control population 5th percentile, and in the range of enzyme activity observed in cells from obligate heterozygotes for inherited acid lipase deficiency (Wolman disease and cholesteryl ester storage disease). Studies of acid lipase activity in families of our patients provided evidence that an autosomal mutation is associated with (or responsible for) this reduced enzymatic activity and may represent an independent risk factor for the premature development of atherosclerosis.
Atherosclerosis 1986 Oct
PMID:Genetic variation of human mononuclear leukocyte lysosomal acid lipase activity. Relationship to atherosclerosis. 377 71

We have studied mechanical factors that could determine how stenosis protects against distal atherosclerosis in cynomolgus monkeys fed an atherogenic diet. Critical aortic stenosis was produced by coarctation of the thoracic aorta. After 3 months, coarcted monkeys had a mean aortic pressure gradient of 25 +/- 1 mm Hg and a 76% +/- 2% lumen stenosis. Aortic wall motion was measured by means of in vivo ultrasonic sonomicrometry. Dynamic tracings of aortic pressure and diameter were recorded simultaneously at standard locations proximal and distal to the stenosis and at comparable sites in noncoarcted control animals. In the proximal aorta, mean blood pressure and pulse pressure were increased (p less than 0.05), but wall motion and intimal lesion area were not different from those determined in control monkeys. In the aorta distal to the coarct, mean blood pressure was no different from that in control animals but pulse pressure was diminished; in addition, there was marked reduction of arterial wall motion (p less than 0.001). This was accompanied by a significant reduction of intimal plaque area (p less than 0.05) and acid lipase activity (p less than 0.001). Thus, inhibition of plaque formation in the distal aorta coincided with reduction of pulse pressure and aortic wall motion rather than with blood pressure or hypercholesterolemia. Inhibition of arterial wall motion may account for the sparing effect often encountered in human arteries distal to stenosing atherosclerotic plaques.
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PMID:Protection from atherosclerotic lesion formation by reduction of artery wall motion. 379 93

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

Purified acid lipase was previously shown to hydrolyze the artificial substrate, alpha-naphthyl palmitate, as well as triglycerides and cholesteryl esters and to form cholesteryl esters. To determine to what extent these activities are associated with acid lipase-containing cells in atherosclerotic plaques, we examined rabbit aortas at different stages of experimental lesion induction and human atherosclerotic arteries. Assays of cholesteryl ester formation, and alpha-naphthyl palmitate and cholesteryl ester hydrolysis were performed on homogenates of lesions and the hydrolysis of the artificial fatty acid ester was used as a histochemical marker to identify acid lipase positive foam cells in sections of the same lesions. The volume of lesions occupied by cells stained for acid lipase correlated strongly with the enzyme activities of the arterial homogenates. These results suggest that acid lipase-containing cells may mediate the accumulation of cholesteryl ester during atherogenesis. Since acid lipase activity marks macrophages, these methods may be useful for relating macrophage distribution and function to lesion progression, regression, and complication.
Atherosclerosis 1985 May
PMID:Role of acid lipase in cholesteryl ester accumulation during atherogenesis. Correlation of enzyme activity with acid lipase-containing macrophages in rabbit and human lesions. 400 91


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