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)

Twelve male patients with mild essential hypertension were put on a diet supplemented with 2 cans of mackerel/day (= 2.2 g daily of eicosapentaenoic acid, EPA, C20:5 n-3 and 2.8 g daily of docosahexaenoic acid, DHA, C22:6 n-3) for 2 weeks within an isocaloric regimen and then with 3 cans/week (= 3.3 g/week, equivalent to 0.47 g daily of EPA and 4.2 g/week, equivalent to 0.69 g daily of DHA) for 8 months with a subsequent period of 2 months on normal diet. Eleven male hypertensives matched for age, body weight index, blood pressure and serum lipids with no change in their nutritional habits served as controls. After the first dietary period (2 weeks) a significant decrease of serum triglycerides (TG), total and LDL-cholesterol, blood pressure and thromboxane B2 (TxB2) was found, whereas HDL cholesterol and potassium in erythrocytes were significantly increased. During the second dietary period (8 months) providing the lower dose of EPA, serum lipids and the other biochemical parameters returned to the initial values. Blood pressure, however, remained significantly lower and rose to the basal levels only after the third period (2 months) on normal diet. In the control group no alterations could be seen. The data suggest a dose-related differential effect of dietary EPA on serum lipids, lipoproteins, TxB2 and blood pressure in subjects with mild hypertension.
Atherosclerosis 1986 Dec
PMID:Long-term effect of mackerel diet on blood pressure, serum lipids and thromboxane formation in patients with mild essential hypertension. 302 12

The consumption of long chain polyunsaturated fatty acids by fish oils leads to profound lowering of plasma triacylglycerol but not of plasma cholesterol. Reasons for this were investigated with the human hepatoma cell line, the Hep G2 cell. Incubations with oleic acid (18:1 n9), linoleic acid (18:2 n6) and the characteristic marine fatty acid eicosapentaenoic acid (EPA, 20:5 n3) enriched cellular triacylglycerol mass, though least with EPA. However, secretion of very low density lipoprotein (VLDL) triacylglycerol and apoprotein B (measured by formation from [3H]glycerol and [3H]leucine) was markedly inhibited by EPA. Preincubation with linoleic acid reduced VLDL triacylglycerol but not apo B secretion in comparison with oleic acid which stimulated both. A possible effect on low density lipoprotein (LDL) removal was studied by measuring [125I]LDL binding. Preincubation with either EPA or linoleic acid inhibited the saturable binding of LDL, observed with oleic acid and control incubations. The binding of lipoproteins containing chylomicron remnants was not affected by any of the fatty acids.
Atherosclerosis 1987 Apr
PMID:Eicosapentaenoic acid inhibits the secretion of triacylglycerol and of apoprotein B and the binding of LDL in Hep G2 cells. 303 33

The influence of a dietary supplement of n-3 polyunsaturated fatty acids containing eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) on the molecular species of cholesteryl esters (CE) formed via the plasma lecithin (phosphatidylcholine)-cholesterol acyltransferase (LCAT; EC 2.3.1.43) reaction was evaluated. For this purpose, one group of eight subjects received an encapsulated fish lipid concentrate (MaxEPA) and another group of eight volunteers in the control group received encapsulated olive oil for 22 days. Plasma lipid profiles and fatty acid compositions of plasma phosphatidylcholine (PC) and CE were measured at day 0 and day 22 in all subjects. A decrease in plasma triglyceride (by 34%) and a moderate rise in high-density lipoprotein (HDL)-cholesterol (by 13%) was observed in the MaxEPA group. For characterization of the plasma LCAT-derived reaction products formed in vitro, [14C]cholesterol was used as the substrate and the newly formed molecular species of [14C]CE were separated by argentation thin-layer chromatography. Marked shifts were found in the abundance of the various classes of LCAT-derived products in the MaxEPA group whereas no significant changes were observed in the controls. The proportion of the [14C]CE as pentaenoic (EPA) species rose by 9-fold (from 1.5% at day 0 to 14.4% at day 22) as the dienoic (linoleate) species fell (from 50.6 to 39.2%); a moderate rise in the hexaenoic (DHA) species (from 1.7 to 2.4%) with no significant change in the tetraenoic (arachidonate) (AA) species was observed. The LCAT results were in the order of the observed shifts in the fatty acid patterns of the plasma CE.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1987 Jul
PMID:Alterations in molecular species of cholesterol esters formed via plasma lecithin-cholesterol acyltransferase in human subjects consuming fish oil. 363 42

Three species of nonhuman primates were fed an atherogenic diet for 6 months (baseline period) and a menhaden oil (EPA)-containing diet for 8 weeks (test period) during which various hemostatic and lipid parameters were compared. The EPA-rich diet prolonged bleeding times, inhibited platelet aggregation response to ADP and collagen, and increased mean platelet lifespan. This diet elicited an increase in the polyunsaturated fatty acids C20:5 (EPA) and C22:6 (docosahexaenoic acid) at the expense of C18:2 (linoleic acid) and C20:4 (arachidonic acid) in pooled samples of platelet membranes, creating an increase in the ratio of n-3/n-6 polyunsaturated fatty acids. The serum lipid response to a menhaden oil diet comprised a nonsignificant decrease in total serum cholesterol and a significant decrease in HDL cholesterol.
Atherosclerosis 1985 Nov
PMID:The effect of a menhaden oil-containing diet on hemostatic and lipid parameters of nonhuman primates with atherosclerosis. 408 62

Twelve volunteers (mean age, 60.7 +/- 4.2 years) were treated with placebo for the first week and then given partially purified eicosapentaenoic acid (EPA, 67% purity) at 2 g per day for 4 weeks. Significant decreases in ADP-, collagen- and adrenalin-induced platelet aggregation were observed at 2 and 4 weeks after EPA treatment, together with an increase in the plasma ratio of EPA to arachidonic acid and in platelet phospholipids. It was concluded that the administration of partially purified EPA was effective in decreasing platelet aggregation, possibly by changing the platelet ratio of EPA to arachidonic acid.
Atherosclerosis 1983 Apr
PMID:Effect of eicosapentaenoic acid on the platelet aggregation and composition of fatty acid in man. A double blind study. 630 22

Fifteen healthy volunteers were put on a mackerel and herring diet, consisting of a prescribed daily isocaloric regimen in a cross-over design, for 2 weeks. Eicosapentaenoic acid (EPA - C20:5, n-3) was predominantly incorporated into cholesterol esters, whereas docosahexaenoic acid (C22:6, n-3) appeared more in serum triglycerides, indicating that the function of the latter may be different from that of EPA. After mackerel ingestion, serum triglycerides, total cholesterol and lecithin cholesterol acyl transferase (LCAT) activity were significantly decreased, returning to basal levels 3 months later. Low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol and postheparin lipolytic activity (PHLA) remained unchanged at the end of the mackerel diet. Generally, after the herring diet the differences were minor, only LCAT activity being significantly decreased. A markedly lower systolic and diastolic blood pressure at the end of the mackerel period could be observed. After herring diet a slight diminution of blood pressure was not significant. Accordingly, plasma noradrenaline was only significantly decreased at the end of the mackerel period. Dopamine-beta-hydroxylase (DBH) activity in serum had no differences before, during and after the study. From the data presented it can be said that a mackerel diet exerts a beneficial influence on cardiovascular risk.
Atherosclerosis 1983 Oct
PMID:Lipid and blood pressure-lowering effect of mackerel diet in man. 631 95

CD36, a multifunctional adhesion receptor e.g. for thrombospondin and collagen, as well as a scavenger receptor for oxidized low density lipoprotein, is expressed e.g. on platelets and monocytes. By this dual role it might be involved in early steps of atherosclerosis like the recruitment of monocytes and formation of foam cells. We therefore studied the effects of n-3 fatty acids on CD36 expression in human monocytic cells. Incorporation of eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) into cellular phospholipids resulted in a significant reduction of CD36 expression at the mRNA and protein level, whereas arachidonic acid (AA, C20: 4n-6) and linoleic acid (LA, C18:2n-6) tended to increase CD36 expression compared to the control. This specific down-regulation of CD36 by n-3 fatty acids in cells involved in the initiation and progression of atherogenesis and inflammation, represents a further mechanism that may contribute to the beneficial effects of n-3 polyunsaturated fatty acids (PUFA) in these disorders.
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PMID:N-3 but not N-6 fatty acids reduce the expression of the combined adhesion and scavenger receptor CD36 in human monocytic cells. 755

We studied the elasticity and endothelium-dependent relaxation (EDR) of the aorta in 1% cholesterol diet (HCD)-fed rabbits. Furthermore, the effects of ethyl all-cis-5,8,11,14, 17-icosapentaenoate (EPA-E) were examined in this model of atherosclerosis. After 12 weeks of feeding with HCD, the animals showed increase in plasma total cholesterol level, formation of atherosclerotic plaque, decrease in aortic elasticity and impairment of EDR to acetylcholine (ACh). The levels of aortic elasticity in HCD-fed rabbits administered orally with EPA-E (300 mg/kg for 12 weeks) were almost the same as those of rabbits fed a normal diet, although EPA-E showed no effects on the plasma total cholesterol level and formation of atherosclerotic plaque in HCD-fed rabbits. On EDR in response to ACh and cyclic GMP formation in the HCD-fed rabbit aorta, EPA-E improved the impairment of these parameters, but not significantly. Therefore, EPA-E had little effect on the endothelium in this model of atherosclerosis, although EPA-E improved the decrease in the aortic elasticity. Because the levels of aortic elasticity showed no significant correlation with the magnitude of EDR to ACh or the size of atherosclerotic plaque, the decrease of aortic elasticity in this model of atherosclerosis was thought to have little relation to the dysfunction of the endothelium.
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PMID:[Effects of ethyl all-cis-5,8,11,14,17-icosapentaenoate (EPA-E) on elasticity and endothelium-dependent relaxation of the aorta in high cholesterol diet-fed rabbits]. 807 89

Eicosapentaenoic acid, which is one of the n-3 polyunsaturated fatty acids (PUFA), is reported to exert its antithrombotic and anti-atherogenic effect partly through the modulation of vascular cell functions. Vascular smooth muscle cell (VSMC) proliferation plays an important role in the pathogenesis of atherosclerosis. We reported the differential effect of various PUFA on VSMC proliferation. First we established a method for preparing PUFA rich cells in culture to mimic the in vivo situation using PUFA triacylglycerol emulsion. Using these fatty acid rich cells, we found that only EPA and docosahexaenoic acid, although less potent than EPA, inhibited the proliferation of VSMC among the fatty acids tested. This effect of EPA was reversed by the addition of anti-oxidants. It is suggested that production of the oxidized species at a low concentration from EPA inhibited the proliferation of VSMC. This anti-proliferative effect of EPA and DHA on VSMC could partly explain the anti-atherosclerotic effect of marine lipids.
Atherosclerosis 1993 Dec
PMID:Eicosapentaenoic acid and docosahexaenoic acid suppress the proliferation of vascular smooth muscle cells. 814 54

In the experimental studies reported in this review, dietary n-3 fatty acids from fish and fish oil had profound hypolipidemic effects in normal subjects and in hypertriglyceridemic patients with combined hyperlipidemia (type II-b) and types IV and V hyperlipidemia. In these carefully controlled metabolic experiments, dramatic reductions occurred in plasma triglycerides and to a lesser extent in plasma total cholesterol. Reductions in VLDL, chylomicrons, remnants, LDL, apo B, and apo E were also noted. HDL changes varied from subject to subject. These plasma lipoprotein changes occurred in subjects with non-insulin-dependent diabetes mellitus as well, without deterioration of diabetic control. Similar results are reported in two other papers in this volume. Fish oil did not cause deterioration of diabetic control. Whereas the mechanism of the hypolipidemic action of the n-6 rich vegetable oils containing linoleic acid such as corn or safflower oil still remains obscure, the mechanism of the hypolipidemic action of the n-3 fatty acids in fish oil is well documented. The synthesis of triglyceride and VLDL in the liver is greatly reduced by n-3 fatty acids. At the same time, the turnover of VLDL in plasma is shortened. In another study, LDL production was decreased. Combined with other dietary manipulations, such as a reduction in saturated fat and dietary cholesterol, the use of n-3 fatty acids to treat hyperlipidemia, especially hypertriglyceridemia, appears to have a well-supported rationale. Fish oil combined with a low cholesterol, low saturated fat diet has been shown to produce complementary effects. Total plasma cholesterol and LDL cholesterol were lowered by the low cholesterol, low saturated fat diet, whereas plasma triglyceride and VLDL were decreased by the fish oil. In most situations, the use of fish oil supplements should be regarded as pharmacologic therapy, particularly effective in severe hypertriglyceridemic states (e.g., chylomicronemia). However, a lifelong diet rich in fish may be protective against atherosclerosis as well. Further studies are required to delineate exact doses and precise indications for the use of fish oil in different types of hyperlipidemias and to differentiate the effects, if any, of the two major n-3 fatty acids in fish oil, EPA and DHA. The hypolipidemic effects of n-3 fatty acids coupled with their known antithrombotic actions (secondary to changes in prostaglandin secretion, platelet function, inhibition of growth factors, and enhancement of endothelial-derived relaxation factor) appear to have an important potential role in the control of coronary heart disease and other atherosclerotic disorders. Moreover, fish oil may prevent the "chylomicronemia" syndrome of type V hyperlipidemia.
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PMID:N-3 fatty acids from fish oil. Effects on plasma lipoproteins and hypertriglyceridemic patients. 835 38


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