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

We have postulated that the accelerated snythesis of cholesteryl ester in atherosclerotic microsomes may result in part from decreased acyl-CoA hydrolase activity in arterial tissue, because acyl-CoA is a common substrate for both reactions. We have now investigated the influence of nutritional status, type of diet, and diabetes on the acyl-CoA hydrolase activity of otherwise normal aortic microsomes. Fasting rabbits for 16 hr diminished the acyl-CoA hydrolase activity approximately 30%. The activity of this aortic microsomal enzyme in rats maintained on a high-carbohydrate diet for 5 weeks was comparable to the activity observed on a high fat (olive oil) diet. The type of fat in the diet influences the acyl-CoA hydrolase activity: oils containing 77% oleic acid (high-oleic safflower oil) and containing 70% linoleic acid (conventional safflower oil) lowered the aortic microsomal acyl-CoA hydrolase activity in comparison to a more saturated fat (cocoa butter). Aortic preparations of rats made diabetic by streptozotocin exhibited higher acyl-CoA hydrolase activity than the normal. The results show that conditions associated with human atherogenesis (diabetes and saturated fat diet) increase rather than suppress the activity of this arterial enzyme in normal arterial tissues of the rat.
Atherosclerosis 1977 Mar
PMID:Influence of dietary status and diabetes on aortic acyl-CoA hydrolase activity. 13 97

This paper reviews studies relating to the effects of fat unsaturation and fatty acid composition on the development of experimental atherosclerosis in rabbits. The results derived from the feeding of various fats are similar whether one feeds cholesterol or an atherogenic, cholesterol-free semipurified diet. In general, the severity of atherosclerosis is inversely related to the level of fat unsaturation. Two exceptions are cocoa butter which is much less atherogenic than expected, most probably due to its high content of stearic acid, and peanut oil, while relatively unsaturated, is surprisingly atherogenic for rats, rabbits and monkeys. This latter effect is not related to the level (6%) of long-chain saturated fatty acids (arachidic, behenic, lignoceric) present in peanut oil, but rather to its triglyceride structure. Randomization of peanut oil, which modifies its triglyceride structure, significantly reduces its atherogenicity.
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PMID:Dietary fat and experimental atherosclerosis. 195 94

Diets currently used to produce atherosclerotic lesions in mice are often undefined and cause accumulation of fat in the liver and gallstone formation. Therefore, synthetic low and high fat diets of known composition were formulated in this study. A synthetic diet containing 50% sucrose, 15% cocoa butter, 1% cholesterol, and 0.5% sodium cholate was found to produce a depression in high density lipoprotein cholesterol (HDL-C) and an elevation of very low density lipoprotein (VLDL) and low density lipoprotein cholesterol (LDL-C) in the atherosclerosis-susceptible strain, C57BL/6J. This diet was able to consistently produce aortic lesions and led to a decrease in liver damage and gallstone formation. The synthetic low fat diet did not produce HDL-C levels as high as those found in mice fed chow, but resulted in similar VLDL/LDL-C levels. Lipoprotein and apolipoprotein parameters were compared in C57BL/6J and the atherosclerosis-resistant strain, C3H/HeJ, consuming the synthetic low fat or high fat diets. As reported earlier, when consuming a high fat diet C57BL/6J mice have significantly lower HDL-C and apoA-I levels than C3H/HeJ mice. Further analysis shows that the molar ratio of plasma HDL-C to apoA-I is significantly lower in C57BL/6J mice, suggesting that HDL in the susceptible strain has a lower cholesterol-carrying capacity. This conclusion is consistent with the observation that the HDL particle size is smaller for C57BL/6J mice than for C3H/HeJ. Both strains increased their apoE levels when fed the synthetic high fat diet, but C3H/HeJ mice had higher levels of apoE on both diets. The major response to consumption of the high fat diet for both strains was an increase in apoB-48 from 5 micrograms/ml on a low fat diet to 54 and 109 micrograms/ml for C57BL/6J and C3H/HeJ, respectively. ApoB-100 showed minimal response to the high fat diet. The defined high fat diet can be used to study atherosclerosis in the mouse since it produces aortic lesions but reduces or eliminates other pathological changes such as gallstone formation and liver damage.
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PMID:Synthetic low and high fat diets for the study of atherosclerosis in the mouse. 238 Jun 34

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

Elevating fat content from 5 to 20% of diet by weight or extending the feeding period from 6 months to more than 1 year did not substantially alter the fluidity of rabbit plasma lipoprotein lipid domains. Dietary fatty acid saturation was not adequate as a predictor of lipoprotein fluidity. Rabbits fed corn oil, high in polyunsaturated fatty acid content, did not have more fluid lipoproteins than rabbits fed cocoa butter which contains a high level of saturated long chain fatty acids. Order parameters calculated from fluorescence depolarization measurements with diphenylhexatriene (DPH) showed that very low density lipoprotein (VLDL) lipids were in highly fluid or 'liquid' states at or below body temperature. Order parameter data showed transitions from ordered phase to isotropic liquid in low density lipoproteins (LDL) that were heretofore unnoted with DPH fluorescence depolarization measurements. The transition temperature was inversely related to the LDL triglyceride content, indicating probe intercalation between the fatty acyl chains of the core triacylglycerols in VLDL and LDL.
Atherosclerosis 1983 Jul
PMID:Effects of fat level, feeding period, and source of fat on lipid fluidity and physical state of rabbit plasma lipoproteins. 688 6

Rabbits were fed a semipurified, cholesterol-free atherogenic diet containing 40% sucrose, 25% casein, 14% fat, 15% fiber, 5% salt mix and 1% vitamin mix. The fats were corn oil (CO), palm kernel oil (PO), cocoa butter (CB), and coconut oil (CNO). The rabbits were bled at 3, 6, and 9 months and killed at 9 months. Serum lipids of rabbits fed CO were unaffected. Serum cholesterol levels (mg/dl) at 9 months were: CO -- 64; PO -- 436; CB -- 220; and CNO -- 474. HDL-cholesterol (%) was: CO -- 37; PO -- 8.6; CB -- 25.1; and CNO -- 7.0. Average atherosclerosis (arch + thoracic/2) was: CO -- 0.15; PO -- 1.28; CB -- 0.53; and CNO -- 1.60. Cocoa butter (iodine value 33) is significantly less cholesterolemic and atherogenic than palm oil (iodine value 17) or coconut oil (iodine value 6). The difference between the atherogenic effects of cocoa butter and palm oil may lie in the fact that about half of the fatty acids of palm oil are C 16 or shorter, whereas 76% of the fatty acids of cocoa butter are C 18 or longer.
Atherosclerosis 1982 Feb
PMID:Experimental atherosclerosis in rabbits fed cholesterol-free diets. 706 76

The effects of dietary stearic and other saturated fatty acids on the fluidity of the plasma lipoproteins were assessed with fluorescence polarization techniques. Rabbits were maintained on diets containing either cocoa butter, milkfat, coconut oil, or corn oil as the only source of fat. Microviscosities eta, of the lipid regions of plasma very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL) were determined by measuring the anisotropy of fluorescence from the probe 1,6-diphenyl-1,3,5-hexatriene. The microviscosity values followed the sequence eta HDL greater than eta LDL greater than eta VLDL when the lipoproteins were isolated from the plasma of rabbits fed cocoa butter, milkfat, or corn oil, HDL and LDL consist of an invariant phase in the temperature range 0--50 degrees C regardless of diet. VLDL from rabbits fed milkfat, corn oil, or cocoa butter displayed monophasic behavior in the same range, while VLDL, from rabbits fed coconut oil showed a phase transition at 31.9 +/- 3.7 degrees C. Lipoproteins were less fluid in fasted than in non-fasted rabbits and VLDL and LDL from fasted milkfat-fed rabbits showed phase transitions. Despite the fatty acid compositions of the dietary fats, VLDL and LDL were more fluid from rabbits fed cocoa butter than from rabbits fed corn oil; apparently metabolism influences microviscosity.
Atherosclerosis 1980 Mar
PMID:Influence of dietary fats on the fluidity of the lipid domains of rabbit plasma lipoproteins. 736 97

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

Mice that are homozygous for a targeted disruption of the LDL receptor gene (LDLR-/- mice) were fed a diet that contained 1.25% cholesterol, 7.5% cocoa butter, 7.5% casein, and 0.5% cholic acid. The total plasma cholesterol rose from 246 to > 1,500 mg/dl, associated with a marked increase in VLDL, intermediate density lipoproteins (IDL), and LDL cholesterol, and a decrease in HDL cholesterol. In wild type littermates fed the same diet, the total plasma cholesterol remained < 160 mg/dl. After 7 mo, the LDLR-/- mice developed massive xanthomatous infiltration of the skin and subcutaneous tissue. The aorta and coronary ostia exhibited gross atheromata, and the aortic valve leaflets were thickened by cholesterol-laden macrophages. No such changes were seen in the LDLR-/- mice on a normal chow diet, nor in wild type mice that were fed either a chow diet or the high-fat diet. We conclude that LDL receptors are largely responsible for the resistance of wild type mice to atherosclerosis. The cholesterol-fed LDLR-/- mice offer a new model for the study of environmental and genetic factors that modify the processes of atherosclerosis and xanthomatosis.
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PMID:Massive xanthomatosis and atherosclerosis in cholesterol-fed low density lipoprotein receptor-negative mice. 818 21

Epidemiologic studies suggest an inverse association of tea consumption with cardiovascular disease. The antioxidant effects of flavonoids in tea (including preventing oxidative damage to LDL) are among the potential mechanisms that could underlie the protective effects. Other possible mechanisms include attenuating the inflammatory process in atherosclerosis, reducing thrombosis, promoting normal endothelial function, and blocking expression of cellular adhesion molecules. Cocoa and chocolate can also be rich sources of flavonoids. Flavanols and procyanidins isolated from cocoa exhibit strong antioxidant properties in-vitro. In acute feeding studies, flavanol-rich cocoa and chocolate increased plasma antioxidant capacity and reduced platelet reactivity. Based on limited data, approximately 150 mg of flavonoids is needed to trigger a rapid antioxidant effect and changes in prostacyclin. Some dose-response evidence demonstrates an antioxidant effect with approximately 500 mg flavonoids. Brewed tea typically contains approximately 172 mg total flavonoids per 235 ml (brewed for 2 min); hence, consumption of 1 and 3.5 cups of tea would be expected to elicit acute and chronic physiologic effects, respectively. Chocolate is more variable with some products containing essentially no flavonoids (0.09 mg procyanidin/g), whereas others are high in flavonoids (4 mg procyanidin/g). Thus, approximate estimates of flavonoid rich chocolate needed to exert acute and chronic effects are 38 and 125 g, respectively. Collectively, the antioxidant effects of flavonoid-rich foods may reduce cardiovascular disease risk.
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PMID:Evidence that the antioxidant flavonoids in tea and cocoa are beneficial for cardiovascular health. 1179 Sep 62


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