Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vitro effects of prostaglandins E1 and F1alpha on the activity of cholesteryl ester synthetase and cholesteryl ester hydrolase activities of the pigeon aorta were examined. It was found that prostaglandin E1 markedly inhibited the cholesteryl ester hydrolase activity in the supernatant fraction and slightly inhibited the cholesteryl ester synthetase activity. Prostaglandin F1alpha, however, modestly stimulated the cholesteryl ester hydrolase activity both in the microsomal and in the supernatant fraction of the aorta. These observations strongly warrant further studies on the role of prostaglandins in atherogenesis.
Atherosclerosis 1977 May
PMID:Effect of prostaglandins E1 and F1alpha on the activities of cholesteryl ester synthetase and cholesteryl ester hydrolases of pigeon aorta in vitro. 1 25

Cholesterol esterase activity was estimated in homogenates of rat arterial wall using radioactive cholesteryl oleate incorporated into phospholipid vesicles as a substrate. The labeled oleic acid was separated from the ester by addition of benzene-chloroform-methanol mixture. Under these conditions, two pH optima were found at about 4.5 and 7.5. Most of the activities at pH 4.5 and 7.5 were found in the lysosomal and microsomal fraction, respectively. No enzyme activity was detected when the substrate vesicles were prepared with phosphatidylethanolamine or sphingomyelin, but the activity was higher when the substrate vesicles were prepared with phosphatidylserine and highest when they were prepared with phosphatidylcholine. The relationship between enzyme regulation and lipid deposition in the arterial wall is discussed.
Atherosclerosis 1979 Jul
PMID:Studies of cholesterol esterase in rat arterial wall. 3 82

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

A number of agents including a series of 1,3-bis (substituted phenoxy)-2-propanones were screened in vitro for their ability to inhibit hepatic and intestinal microsomal sn-glycerol-3-phosphate acyltransferase and phosphatidate phosphohydrolase. Effective inhibitors reduced in vivo hepatic and intestinal glycerolipid production and with one exception also lowered serum triglyceride levels, suggesting that agents which inhibit potential rate-limiting steps of glycerolipid biosynthesis may be effective hypolipidemic agents. Two compounds, 1-methyl-4-piperidyl bis (p-chlorophenoxy) acetate (Sah 42-348) and 1,3-bis (p-methylphenoxy)-2-propanone were the best inhibitors of glycerolipid biosynthesis and lipid-lowering agents. The lipid-altering effects of both drugs were compared to chlorophenoxyisobutyrate during high fructose intake in rats. Each agent reduced fructose induced glycerolipid biosynthesis and serum triglyceride levels to similar degrees.
Atherosclerosis 1977 Jun
PMID:Hypolipidemic activity of in vitro inhibitors of hepatic and intestinal sn-glycerol-3-phosphate acyltransferase and phosphatidate phosphohydrolase. 19 74

This study is the first to report the effect of conjugated equine estrogens on the acitivity of cholesteryl ester synthetase and cholesteryl ester hydrolases in the aorta. In spontaneously atherosclerosis-susceptible White Carneau pigeons, estrogens significantly decreased (P less 0.01) the activity of cholesteryl ester synthetase and increased (P less than 0.01) the cholesteryl ester hydrolase activity in the microsomal fraction of the aorta. There was no effect on the cholesteryl ester hydrolase activity in the supernatant fraction. The inhibition of cholesteryl ester synthesis and the stimulation of cholesteryl ester hydrolase might be responsible for the decreased content of cholesteryl esters noted in pigeon aorta after estrogen treatment.
 ...
PMID:Effect of estrogens on the acitivities of cholesteryl ester synthetase and cholesteryl ester hydrolases in pigeon aorta. 20 Oct 55

This study for the first time has simultaneously assayed three cholesteryl ester hydrolase activities located in the various subcellular fractions (lysosomal, microsomal, and soluble) of the aorta and their significance in aortic cholesteryl ester accumulation during genetic and cholesterol-fed atherosclerosis is assessed. When the enzyme activities in the aorta of age-matched atherosclerosis-susceptible White Carneau and atherosclerosis-resistant Show Racer pigeons were compared, a decrease in microsomal cholesteryl ester hydrolase activity was found during the period of cholesteryl ester accumulation. However, under cholesterol-fed conditions (which further increase cholesteryl ester accumulation), an increase in lysosomal cholesteryl ester hydrolase activity and a decrease in soluble cholesteryl ester hydrolase activity was found. These studies have documented differences in response in specific cholesteryl ester hydrosases of the aorta to genetic and cholesterol-fed atherogenesis and warrant further studies to investigate the effect of hormonal and dietary factors on the activities of these enzymes.
 ...
PMID:Significance of various cholesterol, ester hydrolases in aorta. 44 26

Activity of microsomal enzymes and the patterns of cholesterol metabolism were studied in mice of WSR/y strain, characterized by spontaneous development of atherosclerosis within the later periods of life, after early postnatal administration of an inductor of the enzymes 3-acetate-16 alpha-isothiocyanopregnenolone (ATCP). Administration of ATCP into newborn mice of SWR/y strain, from the 2nd up to 16th day after birth, led to a stable increase in activity of arylhydrocarbonate hydroxylase (an enzyme participating in unspecific metabolism of drugs), which was observed during the whole experimental period (4 months). The treatment with ATCP caused also a distinct increase in activity of cholesterol-7 alpha-hydroxylase (a key enzyme of cholesterol biotransformation and elimination) as well as a considerable decrease in content of cholesterol and lipoprotein atherogenic fractions in blood serum. The rate of cholesterol biosynthesis was similar both in mice treated with ATCP and in the control animals.
 ...
PMID:[Effect of the early postnatal induction of microsomal enzymes on their activity and the cholesterol content in the blood of adult mice from a hypercholesteremic line]. 47 88

Guinea pigs were fed a semisynthetic diet containing 10% (by weight) cottonseed oil and 1% cholesterol. In response to cholesterol/fat feeding there was an increase in both the unesterified cholesterol (UC) and cholesteryl ester (CE) of the intestinal mucosal cell. Along with the increased cholesterol levels there was a 4-fold increase in the microsomal acylCoA:cholesterol acyltransferase (ACAT) activity after only two days of cholesterol/fat feeding. After 6 days on the experimental diet the ACAT activity was up to 8-fold the activity of the control, and then remained at this level for up to 20 days. The increased ACAT activity was probably not due to increased substrate concentration alone, since the fractional esterification of cholesterol also increased when the cholesterol/fat containing diet was given. There was also an increase in the triglyceride content of the intestinal mucosal cells from guinea pigs on the experimental diet. The mucosal cells of the cholesterol/fat fed animals accumulated varying amounts of lipid droplets, which were without an enveloping membrane, suggesting that the uptake of lipids from the intestinal lumen was higher than the capacity to synthesize and/or secrete lipoproteins. Simultaneously the size and amount of secondary lysosomes increased. A considerable increase in lipid droplets, lipolysosomes, and residual bodies was observed in the lamina propria macrophages while no crystalline clefts were seen.
Atherosclerosis 1979 Nov
PMID:Influence of cholesterol/fat feeding on cholesterol esterification and morphological structures in intestinal mucosa from guinea pigs. 51 36

A study was undertaken to test the hypothesis that an abnormally high concentration of acyl-CoA:cholesterol acyltransferase in atherosclerotic microsomes is partly responsible for augmented esterification of cholesterol. We approached the problem indirectly by measuring the incorporation of radioactivity into cholesteryl ester from [1-14C]palmityl-CoA in normal microsomes after enrichment of their concentration of microsomal free cholesterol to levels characteristic of atherosclerotic microsomes. Elevation of free cholesterol content induced increased cholesterol esterification approximately linearly over the range studied. The cholesterol-esterifying activity of atherosclerotic microsomes was not greater than that of normal microsomes having the same concentration of cholesterol. The results suggest that, with acyl-CoA constant, augmented cholesterol esterification in atherosclerotic microsomes is an effect of high microsomal cholesterol concentrations and not due to an increase in the concentration of the enzyme.
Atherosclerosis 1977 Dec
PMID:Studies of the mechanism of augmented synthesis of cholesteryl ester in atherosclerotic rabbit aortic microsomes. 59 52

When rats were fed a diet containing 0.3% clofibrate or a derivative of this drug, BM 15075, serum cholesterol was lowered within 3-7 days by 26-38%. Both drugs diminished the activity of hydroxymethylglutaryl CoA reductase, the regulatory enzyme of hepatic cholesterol biosynthesis, in rat liver microsomes by about 60% under the same conditions. The decrease in the activity of the enzyme obviously is due to changes in the amount of enzyme protein. Under in vitro conditions microsomal hydroxymethylglutaryl CoA reductase was inhibited competitively by (1.35 mM) clofibric acid (sodium salt) and by BM 15075 (1 mM) with respect to its substrate. These results give evidence that these drugs can affect both, the rate of synthesis and the substrate affinity of hydroxymethylglutaryl CoA reductase.
Atherosclerosis 1978 Jun
PMID:Mode of action of the lipid-lowering agents, clofibrate and BM 15075, on cholesterol biosynthesis in rat liver. 67 16


1 2 3 4 5 6 7 8 9 10 Next >>