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)

The effects of different doses of clofibrate and gemfibrozil on liver size, serum triglyceride concentration and the activities of hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and carnitine acyltransferases were studied in male rats. Both clofibrate and gemfibrozil treatment effectively decreased the fructose-induced hypertriglyceridaemia and increased the liver to body weight ratio. Clofibrate treatment also induced an increase of many times in the activities of mitochondrial alpha-GPD and carnitine acyltransferases, the effect increasing with the dose used. The effect of gemfibrozil on the activities of the enzymes was significantly smaller. There was no correlation between the decrease in serum triglyceride concentration and the changes in the activities of the enzymes. Only clofibrate increased the rate of fatty acylcarnitine oxidation in isolated mitochondria. It is concluded that both drugs increased the size of the rat liver, but that only clofibrate influenced the mitochondrial enzyme activities of mitochondrial carnitine acyltransferases and the accelerated mitochondrial oxidation of fatty acids are not the mechanisms by which these drugs lower serum lipid levels.
Atherosclerosis 1979 Jan
PMID:Effect of clofibrate and gemfibrozil on the activities of mitochondrial carnitine acyltransferases in rat liver. Dose--response relations. 46 13

Differences in the ratio of molecular forms of crystalline glycerol-3-phosphate dehydrogenase (GPD, EC 1.1.1.8) from sceletal muscle and in their primary structure were found in rabbits with experimental atherosclerosis as compared with normal animals. In atherosclerosis the molecular weight of GPD and of its fragments was increased; the amino acid composition of these GPD molecules differs from that of control rabbits as shown by estimation of content of 8 amino acids. Experimental atherosclerosis is apparently related to alteration in the GPD primary structure.
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PMID:[Structure of cytoplasmic glycerol-3-phosphate dehydrogenase in experimental atherosclerosis in rabbits]. 59 98

Distrubances are found in the shuttle transport systems of extramitochonidral hydrogen in the brain of rabbits with experimental atherosclerosis, the catalytical function of glyceraldehyde phosphate dehydrohenase being preserved. A decrease in the activity of cytoplasmatic glycerophosphate dehydrogenase was observed parallel with an increase in the content of glycerophosphate. Deviations from the norm in the malate-aspartate shunt are pronounced in a considerable activation of mitochondrial malate dehydrogenase, inhibition of aspartate amino transpherase, accumulation of oxaloacetate and exhaustion of the malate stock. Beta-Oxybutyrate dehydrogenase activates sharply, the content of acetoacetate increases. The total activity of hexoxokinase in cytoplasm and mitochondria remains practically unchanged.
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PMID:[Generation and transport systems of restored equivalents in rabbit brain tissue under experimental atherosclerosis]. 120 81

A light microscopy study on the localization of enzyme activity within atherosclerotic human intracranial arteries was performed on autopsy material obtained within 4 hours of death. The data suggests that the atherosclerotic process first goes through a proliferative phase and then a degenerative phase culminating in the formation of a plaque. In the proliferative phase, smooth muscle cell proliferation has formed a thickened intima. Tetrazolium reductase, adenosine triphosphatase (ATPase) and adenosine monophosphatase (AMPase) activities are present in these cells, while all dehydrogenases and acid phosphatase activities were weak or not present. As the degenerative phase commences, an area of necrosis, lipid and macrophage accumulation is formed on the lumen side of the elastica. This area increases in size until a plaque is formed. Unsaturated polar and nonpolar lipid, cholesterol, alpha-glycerophosphate dehydrogenase, acid phosphatase, and AMPase activities are associated with these areas and in foam cells, which are often found in the thickened intima of the proliferative phase. Tetrazolium reductase and ATPase activities decrease in the thickened intima as the area of necrosis increases in size, while dehydrogenase activity, except that for alpha-glycerophosphate, remains low or not present. Patterns of enzyme alterations for various stages of the disease process in intracranial arteries, the aorta and coronary arteries suggest a similar, if not identical, progression of the atherosclerotic process, irrespective of known differences in the prevalence of atherosclerosis.
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PMID:A histoenzymatic study of human intracranial atherosclerosis. 426 Jul 21

The status of some dehydrogenases (succinate dehydrogenase, mitochondrial alpha-glycerophosphate dehydrogenase and beta-hydroxybutyrate dehydrogenase) was studied in the course of long-term oral administration of cholesterol to rabbits. The data obtained indicate that within the first weeks of cholesterol administration there was a decrease in enzymatic activity of the dehydrogenases under study that mirrored the impairment of energy function of mitochondria. After experiments were initiated, alimentary hypercholesterolemia led to imbalance of anabolism and catabolism bearing resemblance to the status of oxidative processes in the Krebs cycle. There is every reason to believe that such a complex of changes in the dehydrogenases during hypercholesterolemia is characteristic for the initial stages of atherosclerosis. Elimination of cholesterol from the body by single hemosorption results in a tendency towards making the circulating lymphocytes egress from hypoxia. It is inferred that study of enzymatic activity of dehydrogenases should be used for the diagnosis of and the assessment of therapeutic measures for atherosclerosis under experimental and clinical conditions.
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PMID:[Mitochondrial enzymes in circulating lymphocytes during hemosorption for experimental hypercholesterolemia]. 661 50

The effect of AY-25,712 (2-methyl-2-phenyl-3(2H)-furanone-5-carboxylic acid) on serum lipids, hepatic lipogenesis and biliary cholesterol was investigated in male rats. Based on one-week treatment, the minimal effective dose of AY-25,712 which lowered serum triglycerides was 1 mg/kg/day, and LDL-cholesterol, 5 mg/kg/day. Nicotinic acid produced a similar lipid-lowering profile albeit at 5 times higher doses. AY-25,712 at doses of 2 mg/kg/day and higher significantly increased the ratio of HDL to total cholesterol. Unlike clofibrate, AY-25,712 did not increase liver weight or liver mitochondrial alpha-glycerophosphate dehydrogenase, nor increase biliary cholesterol levels in rats fed a diet containing 2% cholesterol and 0.5% cholic acid. AY-25,712 lowered serum cholesterol, triglycerides and phospholipids in rats rendered hyperlipidemic with Triton WR-1339 and decreased the elevated serum triglycerides in streptozotocin-diabetic rats. [14C]Acetate incorporation into cholesterol by liver homogenate was suppressed in rats given AY-25,712 p.o. for 1 week. The results show that AY-25,712 is a potent LDL-cholesterol- and triglyceride-lowering agent in rats, and that its lipid-lowering profile differs from that of clofibrate but resembles that of nicotinic acid.
Atherosclerosis 1982 Dec
PMID:Evaluation of the lipid-lowering activity of AY-25,712 in rats. 681 76