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

The diurnal variation of intermediary metabolites and hormones was determined, as 24-h profiles, in a group of subjects with mixed hypertriglyceridemia while consuming a diet with excess alcohol and caloric intake (Hyp-I) or after a hypotriglyceridemic diet (Hyp-II), and in normal controls. Alcohol was excluded from the hypotriglyceridemic diet and on the days of the study. Hyp-I subjects showed higher 24-h levels of plasma triglyceride, glucose, insulin, lactate, pyruvate, free fatty acid and glycerol. After the hypotriglyceridemic diet the levels of pyruvate, free-fatty acids and glycerol in plasma were normalized, while triglyceride, insulin and glucose concentrations were significantly reduced but remained still higher than in controls. The elevated lactate concentration in Hyp-I subjects were unaffected by the diet. In Hyp-I subjects free-fatty acids and glycerol levels were not suppressed following the meal, in contrast to controls. After the diet this defect in the suppression of endogenous lipolysis was only partially reversed in Hyp-II subjects. Plasma alanine, total ketone body and glucagon concentrations were unaffected. In conclusion, in mixed hypertriglyceridemia high lactate concentration and a defect in the suppression of endogenous lipolysis after a meal could represent a factor enhancing triglyceride production.
Atherosclerosis 1986 May
PMID:Hormonal and metabolic profiles in patients with alcohol-induced, mixed hypertriglyceridemia before and after abstinence from ethanol and before and after a lipid-lowering diet. 371 12

Ten males (mean age 44 years) with primary hypertriglyceridemia were trained for 4 months 3 times/week for 1-h sessions. Eleven patients with similar physical characteristics and hypertriglyceridemia served as controls. Serum was assayed for TG and cholesterol (CH) and the various lipoprotein fractions, apoprotein A-I, glucose, insulin, and C-peptide. The removal of TG from the circulation was estimated by the Intralipid test. An open fat biopsy was taken and the incorporation and esterification of [14C]palmitate and glycerol release were measured in vitro. Following endurance physical training, serum TG and VLDL-TG decreased by 25 and 27%, respectively. No changes were observed in total CH and CH in the lipoprotein fractions or in apoprotein A-I. Fat tolerance increased slightly (+8%) whereas the incorporation of labelled palmitate into adipose tissue was reduced by 16%. The diminished incorporation was concomitant with a reduction in the esterification of fatty acids to TG (-29%). Enhanced removal of TG may contribute to the lowering of serum TG. The skeletal muscle is probably responsible for this adaptation, whereas the uptake of TG into adipose tissue is diminished.
Atherosclerosis 1985 Mar
PMID:Training-induced changes in serum lipids, fat tolerance, and adipose tissue metabolism in patients with hypertriglyceridemia. 399 82

The concentration of lysophosphatidylcholine (monoacyl sn-glycerol 3-phosphorylcholine) in intima plus inner media of atherosclerotic aorta from squirrel monkeys was nearly eight times that in comparable control tissue. Plasma levels of the same compound were somewhat elevated in the atherosclerotic group. The metabolism of fatty acyl CoA's and lysophosphatides was studied in cell-free preparations of intima plus inner media from squirrel monkey aorta. Linoleic acid was incorporated predominantly into phosphatidylcholine (as opposed to other phospholipids) when linoleoyl-1-(14)C CoA was the substrate. The extent of this reaction was dependent on the concentration of lysophosphatidylcholine. Lysophosphatidylethanolamine (monoacyl sn-glycerol 3-phosphorylethanolamine) stimulated the incorporation of linoleate into phosphatidylethanolamine. 1-Palmitoyl-1'-(14)C sn-glycerol 3-phosphorylcholine ((14)C-lysophosphatidylcholine) was incorporated into phosphatidylcholine only in the presence of acyl CoA's or ATP plus CoA. Incorporation of (14)C with (14)C-lysophosphatidylcholine plus linoleoyl CoA equaled that with linoleoyl-1-(14)C CoA and lysophosphatidylcholine. Various other lines of evidence are presented to support the importance of the fatty acyl CoA:lysophosphatide fatty acyl transferase mechanism in aortic phospholipid metabolism. Cell-free preparations of aortic intima plus inner media from squirrel monkeys with early, nutritionally-induced atherosclerosis utilized linoleoyl-1-(14)C CoA more than preparations from control monkeys when incubations were carried out without added lysophosphatidylcholine and for long periods (30 min). With optimum levels of labeled linoleoyl CoA and unlabeled lysophosphatidylcholine, or unlabeled linoleoyl CoA and labeled lysophosphatidylcholine, there were no differences in substrate utilization between control and atherosclerotic tissues. We conclude that the concentrations of lysophosphatidylcholine, which are higher in atherosclerotic than in control aortic tissues, could be a factor controlling rates of fatty acid incorporation into phosphatidylcholine.
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PMID:Lysophosphatidylcholine concentrations and metabolism in aortic intima plus inner media: effect of nutritionally induced atherosclerosis. 423 47

We have studied the effect of long-term hyperlipemia and atherosclerosis in squirrel monkeys on the metabolism of lysolecithin-(14)C (1-palmitoyl-1'-(14)C sn-glycerol 3-phosphorylcholine) in order to explain elevated plasma and arterial concentrations of lysolecithin. The die-away curves of lysolecithin-(14)C from plasma and the timing of appearances of other (14)C-labeled moieties in plasma and other tissues demonstrated a complex pattern of metabolic reactions. There was a rapid equilibration of specific activities of lysolecithin of plasma, liver, and aortic intima plus inner media. The specific activities of lecithin peaked first in liver, then in plasma, and rose slowly in aortic intima plus inner media. The appearance of lecithin-(14)C in heart and skeletal muscle was also slower than in the liver and some other tissues. Triglycerides, and to a lesser extent, cholesteryl esters contained radioactivity. The concentrations of aortic lysolecithin in the atherosclerotic aortas were several times greater than comparable values for control aortas, and the time of equilibration of plasma and aorta lysolecithin-(14)C was much greater for the atherosclerotic group. The quantities of lysolecithin in plasma and in the pool of which the plasma was a part, were increased with hyperlipemia and atherosclerosis, as was the rate of lysolecithin production in the fast pool. Hyperlipemia was also associated with an early increase in plasma lecithin:cholesterol acyltransferase (LCAT) activity in vitro. Furthermore, nutritional hyperlipemia influenced the distribution of lysolecithin-(14)C and lecithin-(14)C between different plasma lipoproteins. The increase in concentrations of lysolecithin in the aorta occurred more slowly than that in plasma after we had induced hyperlipemia in the monkeys.
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PMID:Metabolism of lysolecithin in vivo: effects of hyperlipemia and atherosclerosis in squirrel monkeys. 499 21

Lipogenesis was measured with glucose-2-(14)C and acetate-1-(14)C in the everted aortas of normal and atherosclerotic rabbits. More glucose-2-(14)C than acetate-1-(14)C was incorporated into lipids in both the normal and the atherosclerotic aorta. Radiocarbon from glucose-2-(14)C appeared mainly in triglycerides and phospholipids with a small amount in cholesteryl esters. Incorporation increased almost threefold with atherosclerosis, most of the radioactivity being in the glycerol moiety; radioactivity was predominantly in carbon 2 of glycerol. About 70% of the acetate-1-(14)C incorporated into phospholipids and triglycerides was in the fatty acids, and the remainder was in glyceride-glycerol; 98% of the radioactivity in cholesteryl esters was in the fatty acid moiety. Incorporation into cholesteryl esters was increased most during the development of atherosclerosis. Fatty acid synthesis was similar from both acetate-1-(14)C and the 2 carbon unit derived from glucose-2-(14)C, viz., predominantly de novo synthesis of fatty acids with 14 and 16 carbon atoms, and elongation for those of 18 carbons and longer.
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PMID:Lipogenesis from glucose-2- 14 C and acetate-1- 14 C in aorta. 512 36

Several investigators have observed increased levels of esterified oleic acid in tissue cholesterol esters and phospholipids of atherosclerotic humans and cholesterol-fed animals. However, the cause of this is still unknown. Increased synthesis, increased esterification, or both of oleic acid can account for this. In the present investigation, hepatic synthesis of oleic acid is studied in cholesterol-fed rabbits. A nearly 3-fold increase in oleic acid synthesis was observed after 3 weeks of cholesterol feeding. This increase continued for at least 6 weeks. Since acyl acceptors like glycerol-3-phosphate are known to increase liver oleic acid synthesis it is possible that the observed increased in oleic acid formation was partially due to an increased availability of acyl acceptors in the system.
Atherosclerosis 1982 Jan
PMID:Increased liver oleic acid synthesis in cholesterol-fed rabbits. 612 54

Dietary lipids can modify the properties of cell membranes, including membrane fluidity and membrane permeability. The saturation and isomerization of dietary fatty acids may affect the pattern of fatty acids acylated to glycerol in phospholipids. Oxidized sterols may affect membrane properties directly by their insertion in the membrane or indirectly through their effects on lipid metabolism. The flow of calcium and other nutrients into the cells appears to be a major property affected by those changes in lipid composition of membranes and may be important in the onset of atherosclerosis. The factors that alter the character of the lipids in cell membranes should receive increased study in both in vitro and in vivo systems to clarify their role in diseases processes.
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PMID:Modification of cell membrane composition by dietary lipids and its implications for atherosclerosis. 636 94

The progestin, levonorgestrel administered orally to fed female rats significantly lowers both plasma total and very low density lipoprotein triglycerides. In contrast, plasma total cholesterol and low density lipoprotein cholesterol rose significantly. Suspensions of isolated hepatocytes were used to study the effects of levonorgestrel on triglyceride synthesis by examining the incorporation of labelled precursors [( 9,10- 3H]palmitate and [U-14C]glycerol) into triglycerides. Levonorgestrel (10(-4) M) significantly inhibited the incorporation of both precursors into hepatocyte triglycerides and also reduced their incorporation into the triglycerides (nearly all in d less than 1.006) released into the medium. These results suggest that inhibition of hepatic triglyceride synthesis and release can account at least for part of the lowering of plasma VLDL which occurs during administration of levonorgestrel.
Atherosclerosis 1984 Sep
PMID:Hypotriglyceridemic effects of levonorgestrel in rats. 643 17

The progestin, norethindrone acetate has been widely administered to patients in the form of oral contraceptives; however, its hypolipemic action has received little study. This report describes the effects of conventional doses of norethindrone acetate (100 micrograms/day.kg body weight 0.75) on rat plasma lipid levels in vivo as well as the mechanism of action on triglyceride metabolism in isolated hepatocytes in vitro. Norethindrone acetate administration led to significant and proportional reductions of the concentrations of triglycerides, cholesterol and phospholipids of plasma lipoproteins of density less than 1.006 of rats fed a high carbohydrate diet. Norethindrone acetate (0.1 mM) also significantly inhibited the incorporation of both [9,10(-3)H] palmitate and [U-14C]glycerol into triglycerides of isolated hepatocytes from fed rats, by 11 to 16% (P less than 0.001). Release of labeled triglycerides from the isolated hepatocytes was similarly inhibited, 21% and 46%, respectively (P less than 0.05). At the higher concentration of 1.0 mM, norethindrone acetate inhibited the incorporation of [2(-3)H]glycerol into hepatocytic triglycerides by 35-39% (P less than 0.05). The present findings suggest that inhibition of hepatic triglyceride synthesis can account for the reduction of hepatic triglyceride secretion and for at least part of the lowering of plasma VLDL levels which occurs during administration of norethindrone acetate in the rat.
Atherosclerosis 1983 Jan
PMID:Norethindrone acetate inhibition of triglyceride synthesis and release by rat hepatocytes. 683 93

The activity of cholesterol ester hydrolase was measured in subcellular fractions from rat and pigeon aortas using a glycerol-dispersed cholesterol oleate substrate preparation. The specific activity of acid cholesterol ester hydrolase (assayed at pH 5) in adventitia tissue fractions was 40-50 fold greater than in media-intima fractions from rat aorta. Soluble and particulate subcellular fractions from rat aorta (media-intima) were observed to have cholesterol ester hydrolase activity with both an acid (pH 4.5-5) and a neutral (pH 7.5) pH optimum. A comparison of the subcellular distribution of acid cholesterol ester hydrolase with the lysosomal marker enzyme, N-acetylglucosaminidase, suggests that the acid hydrolase activity originated in aortic lysosomes; the neutral cholesterol ester hydrolase was predominantly soluble. Acid and neutral cholesterol ester hydrolases could also be distinguished on the basic of the effects of Mg Cl2 and NaCl on hydrolase activity and on rates of thermal denaturation. Both acid an neutral hydrolases from rat aorta (media-intima) were inhibited by chloroquine (half-maximal at 2-4 mM), and both hydrolases were characterized as having the same apparent affinity for the glycerol-dispersed cholesterol oleate substrate. Acid and neutral cholesterol ester hydrolases were also observed in preparations from pigeon aortas. The specific activity for both acid and neutral hydrolases was higher in atherosclerosis-susceptible White Carneau pigeon aortas in comparison to Show Racer pigeon aortas.
Atherosclerosis 1982 Jan
PMID:Properties of acid and neutral cholesterol ester hydrolases in rat and pigeon aortas. 707 88


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