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

Feeding natural fats varying in contents of palmitate (16:0), stearate (18:0), oleate (18:1), and linoleate (18:2) to rabbits resulted in modulation of platelet phospholipid fatty acyl composition. Rabbits were fed high fat semipurified diets containing 2% corn oil (CO) + 18% CO, cocoa butter (CB) or milkfat (M) for periods of up to 300 d. Platelet phospholipid linoleate contents corresponded to diet levels with 18:2 highest in CO-fed rabbits and following the sequence CO greater than CB greater than M. Stearate was highest in CB-fed rabbits, corresponding to high 18:0 levels in CB, but palmitate levels were not affected by diet. Both CB and M-fed rabbits were higher than CO-fed rabbits in oleate. Though CO is highest in 18:2, the accepted 20:4 precursor, arachidonate was highest in M-fed rabbits. Adding cholesterol (0.2%) to the diets did not affect platelet phospholipid fatty acyl composition except to elevate 20:4 in M-fed rabbits. CO-fed rabbits showed uniquely high levels of tetracosadienoate (24:2). Fatty acyl composition data were essentially constant between 200 and 300 d on diet. Phospholipid fatty acyl unsaturation was apparently homeostatically controlled as mole percent unsaturate to saturate ratios were independent of diet. The observed homeostasis resulted in minimal diet influences on platelet membrane fluidity and ADP or collagen stimulated platelet aggregation. Platelet fluidity, determined by fluorescence polarization, was a function of oleate and linoleate contents of the cells. Cholesterol feeding generally lowered platelet fluidity and altered the dependence of fluidity on fatty acyl composition.
Atherosclerosis 1987 Jan
PMID:Influence of saturated and unsaturated fats on platelet fatty acids in cholesterol-fed rabbits. 382 74

Electron paramagnetic resonance with the use of stearic acid derivatives (5- and 16-doxylstearate) as spin probes was applied to studies of the structural organization of rabbit platelets in experimental atherosclerosis. Substantial differences were established in the molecular packing of phospholipid plasma membranes, associated with a higher molar content of cholesterol in the cells. An increase in the aggregation properties of platelets was also observed, manifesting in a shorter time of the ADP-induced aggregation of platelets isolated from plasma. The data obtained confirm the primary part of membranotropic cholesterol activity in atherosclerosis, attesting to the validity of the "membraneous" hypothesis of the atherogenesis.
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PMID:[Structural and functional changes in thrombocytes in experimental atherosclerosis]. 632 Sep 26

The fatty acid composition of the cholesteryl esters in serum was measured in 7- and 8-year-old boys in groups from 16 countries. The ratio of esterified cholesterol: total cholesterol was also measured. All sample collections and analyses were carried out under standardized conditions. The proportion of palmitic acid in the cholesteryl esters was high in the groups from Asia and Africa (0.17-0.26) compared with that in the groups from the U.S.A. and Europe (0.14-0.18). The proportion of linoleic acid in the cholesteryl esters was low in the groups from Asia and Africa (0.39-0.48) and high in the groups from the U.S.A. and Europe (0.45-0.58). The proportion of oleic acid, arachidonic acid, palmitoleic acid and stearic acid showed little variation between the groups. The proportion of linoleic acid in the cholesteryl esters was positively correlated with the concentration of total cholesterol (r = 0.75, n = 26, P < 0.005).
Atherosclerosis 1980 Dec
PMID:Fatty acid composition of cholesteryl esters in serum in boys from 16 developing and developed countries. 745 4

To elucidate the direction and magnitude of effects of nutrition on coronary artery disease (CAD), the relation between nutrient intake and angiographic changes were examined in the course of a controlled dietary trial. Ninety men with symptomatic CAD and serum cholesterol greater than 232 mg/dL were entered into a randomized controlled trial of a lipid-lowering diet, or of diet plus cholestyramine, compared with usual cardiac care. Of those in the first and second groups, 50 patients completed the trial and are the subject of this report. Quantitative coronary angiography was performed at baseline and at 39 months. From repeated dietary assessment during the trial, mean nutrient intakes were computed, and their relationships with change of coronary artery narrowing were analyzed. Progression of coronary disease was directly, strongly and independently associated with intake of saturated fatty acids of chain length 14-18. This was not fully explained by the effects of saturated fat in raising serum cholesterol; after adjustment for low density lipoprotein cholesterol level, stearic acid (C18:0) intake remained independently predictive of progression. No 'protective' effect of linoleic, linolenic or eicosapentaenoic acid was demonstrable. Intake of trans fatty acids was directly related to progression. Together with the favourable treatment effects on angiographic appearance and clinical end-points, these findings provide further support for a causal role of saturated fats in CAD; restriction of foods containing such fats should be emphasized as part of regimens aimed to reduce progression of coronary atherosclerosis.
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PMID:Relationships between nutrient intake and progression/regression of coronary atherosclerosis as assessed by serial quantitative angiography. 758 83

Endothelial cell dysfunction has been implicated in the development of atherosclerosis. Of vital importance to the maintenance of endothelial cell integrity is the preservation of membrane functional and structural properties, such as membrane fluidity. The aim of this study was to develop a model for studying the relationship between endothelial cell integrity and membrane fluidity alterations in a well-defined cell culture setting. Alterations in membrane fluidity were assessed using electron spin resonance after labeling endothelial cells with the lipid-specific spin labels, CAT-16 and 12-nitroxide stearic acid. Endothelial cells were exposed to various 18-carbon fatty acids, i.e. stearic (18:0), oleic (18:1), linoleic (18:2), or linolenic (18:3), in addition to lipolyzed HDL (L-HDL) and benzyl alcohol. Membrane phospholipid fatty acid composition of endothelial cells supplemented with these fatty acids was analyzed using gas chromatography. All fatty acids, except 18:0, decreased membrane fluidity. A relationship between membrane fluidity and fatty acid compositional alterations in cellular phospholipids was observed. In particular, the arachidonic acid content decreased following exposure to 18:1, 18:2, or 18:3. Exposure of endothelial cells to L-HDL, lipoprotein particles which contain high levels of 18:1 and 18:2, also decreased membrane fluidity. The stabilization of cytoskeletal actin filaments by phalloidin partially prevented 18:2-induced increases in albumin transfer, thus implicating a cytoskeletal involvement in the 18:2-induced membrane fluidity changes involved in endothelial cell dysfunction. The present study shows that the exposure of endothelial cells to various lipids causes membrane fluidity alterations which may contribute to endothelial cell dysfunction and atherosclerosis.
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PMID:Electron spin resonance studies of fatty acid-induced alterations in membrane fluidity in cultured endothelial cells. 764 22

The average diet may provide some 8-10 g/day of unsaturated fatty acids with a trans double bond. Previous studies showed that dietary trans fatty acids may simultaneously raise low-density lipoprotein (LDL) cholesterol and reduce high-density lipoprotein (HDL) cholesterol. Human plasma contains a protein (CETP) which transfers cholesterylesters from HDL to lipoproteins of lower density. We hypothesized that CETP could play a role in the effect of trans fatty acids on lipoproteins and measured the activity levels of CETP in serum samples from a 9-week study in which 55 volunteers were fed three controlled diets with different fatty acid profiles. Mean activity was 114 (% of reference serum) after consumption of a high trans fatty acid diet, as opposed to 96 after linoleic acid and 97 after stearic acid (P < 0.02). We conclude that the increased activity of CETP may contribute to the rise in LDL cholesterol and the fall in HDL cholesterol seen on diets with high contents of trans fatty acids.
Atherosclerosis 1995 May
PMID:Dietary trans fatty acids increase serum cholesterylester transfer protein activity in man. 864 66

Evidence continues to accumulate that implicates the oxidative modification of low-density lipoprotein (LDL) in the pathogenesis of atherosclerosis. Numerous studies have indicated the existence of oxidized LDL in vivo. Supplementation of animals and humans with antioxidants such as alpha-tocopherol have shown promise in reducing the extent of LDL oxidation. However, another possible means of preventing LDL oxidative modification may be by reducing the amount of oxidizable polyunsaturated fatty acids in the LDL particle. Monounsaturated fatty acids have been shown to decrease the susceptibility of LDL oxidation in human studies. It remains to be seen whether saturated fatty acids can do the same. Stearic acid, found in cocoa butter, would be an ideal saturated fatty acid to test because it has a neutral effect on the plasma lipid profile.
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PMID:Effects of antioxidants and fatty acids on low-density-lipoprotein oxidation. 797 41

Endothelial cell integrity has been suggested to play a role in the development of atherosclerosis. The effects of fatty acids on endothelial barrier function were tested by measuring albumin transport across endothelial monolayers cultured on polycarbonate filters. Compared with control cultures, a 24-h exposure to 90 mumol/L lauric (12:0) and linoleic acid (18:2) but not to butyric (4:0), hexanoic (6:0), octanoic (8:0), decanoic (10:0), myristic (14:0), palmitic (16:0) or stearic acid (18:0) caused an increase in albumin transfer across endothelial monolayers. Selective enrichment of a "physiological" serum fatty acid mixture (FA-Mix; 90 mumol/L) with 90 mumol/L of 12:0 or 18:2 significantly increased albumin transfer, whereas enrichment with 90 mumol/L of 4:0, 16:0 or 18:0 significantly decreased albumin transfer relative to 180 mumol/L FA-Mix. Only 12:0- or 18:2-treated cultures showed increased Ca(++)-ATPase activity and the presence of lipid droplets. Fatty acids (60 mumol/L) extracted from butter fat and beef tallow had no effect on albumin transfer, whereas fatty acids extracted from chicken fat and corn oil consistently disrupted endothelial barrier function. This fat-induced disruption of endothelial barrier function seems to be related to the amount of 18:2 present in each fat source. These data indicate that unsaturated fats cause cellular perturbations that result in a decrease in endothelial barrier function in this model system, and that high dietary levels of unsaturated fats may be detrimental to cell integrity.
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PMID:Selective disruption of endothelial barrier function in culture by pure fatty acids and fatty acids derived from animal and plant fats. 832 May 62

We studied the effects of addition of physiological concentrations (0.5 mM) of fatty acids i.e., palmitic (16:0), stearic (18:0), oleic (18:1) and linoleic acid (18:2) on lipoprotein secretion by polarized Caco-2 cells. With saturated fatty acids, secreted lipoproteins were at IDL/LDL density, 1.009 < d < 1.068 g/ml. The numbers of secreted lipoproteins, expressed as secreted apolipoprotein (apo) B, were comparable to control without fatty acid (palmitic acid, 551 +/- 185; stearic acid, 629 +/- 304 and control, 504 +/- 176 ng apo B/4.7 cm2 filter). With unsaturated fatty acids, apo B containing lipoproteins were secreted at chylomicron/VLDL density (d < 1.006 g/ml). Oleic acid caused a two-fold higher secretion of apo B than control (1058 +/- 87 vs. 504 +/- 176 ng/4.7 cm2 filter, P < 0.001). The increase in apo B secretion was attributed to a specific increase in apo B-48. Unsaturated fatty acid caused a two-fold higher secretion of triglyceride than saturated fatty acids but incorporation of newly synthesized lipid into the secreted lipoproteins, measured by incorporation of a fatty acid marker, was 10- to 20-fold higher, indicating preferential translocation of unsaturated triglycerides into lipoproteins. Mixtures rich in either polyunsaturated, monounsaturated, or saturated fatty acids, resembling nutritional fat and oils, were capable of a two-fold stimulation of secretion of apo B containing triglyceride-rich lipoproteins. The triglyceride/apo B ratio in the basolateral medium was higher with the monounsaturated 'olive oil' mixture (12 250 +/- 2000 mol/mol) than with the polyunsaturated 'corn oil' mixture (7830 +/- 2480 mol/mol) and incorporation of newly synthesized lipid into the secreted lipoproteins was 1.5-fold higher as well. In conclusion, unsaturated fatty acids were most potent in stimulating the secretion of apo B by specifically increasing apo B-48 secretion. Unsaturated triglycerides, that contain mainly oleic acid, were more efficiently incorporated into lipoproteins than saturated triglycerides, suggesting preferential translocation by microsomal triglyceride transfer protein.
Atherosclerosis 1996 Mar
PMID:Effects of saturated, mono-, and polyunsaturated fatty acids on the secretion of apo B containing lipoproteins by Caco-2 cells. 867 19

Epidemiological studies have identified high heart rates as a risk factor for coronary heart disease mortality, and heart rate was found to correlate with the severity of coronary atherosclerosis. Heart rate was positively correlated with serum concentrations of total cholesterol, triglycerides, and non-HDL cholesterol. Since heart rate responds sensitively to sympathoadrenergic activity, it was hypothesized that catecholamines play a crucial role in the unfavorable lipid alterations. In addition to influences on circulating lipids, the question arose whether catecholamines have more specific effects on molecular species of structural lipids. Of particular importance is the question of the involvement of catecholamines in the recently suggested correlation between arachidonic acid and stroke mortality. It is therefore attempted to delineate the possible effects of catecholamines on the fatty acid composition of the phospholipids of heart muscle and vasculature. This was achieved in rats by either catecholamine injection or by swimming, a condition known to be associated with marked sympatho-adrenergic stimulation. In swimming rats, linoleic acid was decreased by up to 40% in heart phospholipids, whereas stearic acid and arachidonic acid were increased. Similarly, chronic norepinephrine treatment in rats resulted in a net decrease in linoleic acid and an increase in arachidonic acid and docosahexaenoic acid, which was particularly pronounced when rats were fed an n-3 polyunsaturated fatty acid (PUFA)-rich oil diet. Thus, catecholamines do affect the PUFA composition of heart membranes, mainly through an increase in arachidonic acid content. To further define the action of catecholamines on structural lipids, isolated rat ventricular myocytes in culture were subjected four times to 30 minutes of isoproterenol (10(-6) M) stimulation over 48 hours. No changes in membrane lipid parameters were observed, although the beating rate was increased by 30% during the stimulation. When the cell membranes were enriched in n-3 PUFAs (in association with a decrease in arachidonic acid), the positive chronotropic effect elicited by isoproterenol was raised to + 50%, indicating the modulation of adrenergic function by membrane PUFAs. However, isoproterenol treatment again had no effect on the phospholipid fatty acid composition. Thus, the effect of catecholamines on membrane lipids observed in intact organism appears to be indirect and to involve most probably organs such as the liver and adipose tissue. Catecholamines are expected to induce a lipolysis-linked quantitative and qualitative alteration in circulating fatty acids, which in turn alter the heart membrane composition, similar to the composition changes elicited by diet lipid alterations. Since there is increasing evidence that such fatty acid changes affect the activity of membrane proteins, the possibility emerges that this mechanism may contribute to the catecholamine-linked cardiovascular mortality.
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PMID:Sympathoadrenergic overactivity and lipid metabolism. 882 44


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