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)

Accelerated atherosclerosis is a major complication of long-term diabetes mellitus, and this is partly due to associated abnormalities of lipoprotein metabolism. Hypertriglyceridemia is usually due to poorly controlled diabetes and responds to improved glucose control. Hypercholesterolemia is usually not related to poor diabetic control and should be treated with a cholesterol lowering diet and drugs according to the National Cholesterol Education Program guidelines. Low HDL-C is common in NIDDM and does not fully return to normal with improved diabetic control. Dyslipidemia in diabetics should be aggressively identified and treated to decrease cardiovascular risk.
 ...
PMID:Management of hyperlipidemia in diabetes mellitus. 161 72

It has been supposed that prostacyclin (PGI2) and its analogues have important antiatherogenic effects. The aim of this work was to test the effect of PGI2 and 7-oxo-PGI2- (a stable analogue of PGI2) (6) treatment on the acyl CoA: cholesterol-acyltransferase (ACAT) activity in the aortic wall of rabbits. The rabbits had been previously fed with cholesterol and treated with PGI2 and 7-oxo-PGI2 intravenously. Cholesterol feeding increased ACAT activity compared to the control group which was not fed with cholesterol: 16.84 nmol/mg prot./h and 10.03 nmol/mg prot./h, respectively. PGI2 treatment of the cholesterol fed group did not cause a significant decrease, while 7-oxo-PGI2 treatment significantly decreased aortic ACAT activity compared to the cholesterol-fed control group; 14.31 nmol/mg prot./h; 11.53 nmol/mg prot./h and 16.84 nmol/mg prot./h, respectively. The decrease found in the ACAT activity after PGI2 and 7-oxo-PGI2 treatment are new data for the protective effect of these agents against atherosclerosis.
 ...
PMID:Inhibition of ACAT activity after 7-oxo-PGI2 treatment in cholesterol-fed rabbits. 161 86

Decreased acid cholesterol esterase has been linked to cholesteryl ester accumulation and may be fundamental in the development of atherosclerosis. The present study compared cholesterol esterase activity with the accumulation of cholesterol and its esters in aorta, renal artery and renal preglomerular microvessels. Tissue was obtained from white New Zealand rabbits fed either a control or 2%-cholesterol diet for 1 month. Cholesterol esterase was increased in microvessels from cholesterol-fed animals when compared to aorta and renal artery. Cholesterol feeding generally produced an increase in cholesterol and cholesteryl ester accumulation in all vascular tissues. The percent distribution of esterified/total cholesterol in renal microvessels was decreased consistent with the concomitant increase in cholesterol esterase. In contrast, aorta and renal artery exhibited an increase in cholesterol and cholesteryl ester accumulation and an increase in the percent of esterified cholesterol consistent with a decrease in acid cholesterol esterase after cholesterol feeding. The data suggest that renal microvessels, when compared to aorta and renal artery, may be relatively protected from developing atherosclerotic microvascular lesions through an organ-specific increase in acid cholesterol esterase activity.
Atherosclerosis 1992 May
PMID:Comparative studies on acid cholesterol esterase in renal blood vessels and aorta of control and hypercholesterolemic rabbits. 163 56

We describe the first Finnish LCAT-deficient family with two affected, one questionably affected and one healthy family member. The affected family members presented stomatocytes in the peripheral blood, exhibited low serum levels of total, LDL and HDL cholesterol, triglycerides, phospholipids and apolipoprotein A-I and especially A-II. Apolipoprotein A-I catabolism was accelerated to moderately high and very high levels in the two affected subjects. Cholesterol esterification percentage was low in all lipoprotein fractions. The intestinal cholesterol absorption efficiency and cholesterol and bile acid synthesis were within normal limits. The esterification percentage of demethylated cholesterol precursor sterols, cholestanol and plant sterols resembled mostly that of cholesterol, while those of VLDL and LDL methostenols, precursor sterols esterified by acyl-CoA:cholesterol acyltransferase (ACAT), suggested normal ACAT activity. In HDL all sterols were poorly esterified. The observations on stomatocytes, normal absorption and synthesis of cholesterol and bile acids, abnormal kinetics of apolipoprotein A-I, evidence of normal ACAT activity and abnormal esterification of non-cholesterol sterols are findings presented for the first time in LCAT deficiency.
Atherosclerosis 1992 Jul
PMID:Non-cholesterol sterols, absorption and synthesis of cholesterol and apolipoprotein A-I kinetics in a Finnish lecithin-cholesterol acyltransferase deficient family. 164 89

Data from two epidemiological studies are used to measure the degree to which two well-known guidelines agree in measuring hyperlipidemia in population samples in the US and Poland. The epidemiological studies are the US Lipid Research Clinics Program Prevalence Study and the Pol-MONICA project in Poland and the guidelines are those adopted by the US National Cholesterol Program (USNCEP) and by the European Atherosclerosis Society (EAS). EAS guidelines were analyzed in two ways: Method 1 used triglycerides and total cholesterol only in classifying persons as hyperlipidemics or non-hyperlipidemics; Method 2 used triglycerides, total cholesterol and nine additional risk factors in the classification process. USNCEP guidelines used total cholesterol, low density lipoprotein cholesterol and the same additional nine risk factors used in EAS Method 2 in classifying hyperlipidemics. Classification differences between the two sets of guidelines were high when EAS Method 1 guidelines were compared with USNCEP guidelines. However, EAS Method 2 which included risk factors, compared favorably with USNCEP guidelines in all three populations under study.
Atherosclerosis 1992 Jul
PMID:Poland-US collaborative study on cardiovascular epidemiology: classification agreement between US National Cholesterol Education Program and European Atherosclerosis Society hyperlipidemia guidelines in selected Polish and US populations. 164 91

The content of 13-hydroxylinoleic acid (13-HODE) and 15-hydroxyarachidonic acid (15-HETE) in the rabbit thoracic aorta was measured using high performance liquid chromatography after chronic exposure to cholesterol and a high dose of molsidomine, a donor of nitric oxide (NO). Cholesterol-induced fatty streak formation was accompanied by a decrease in the amounts of esterified 13-HODE and 15-HETE. The reduction of the esterified 13-HODE content correlated significantly with the severity of the lesions. These results do not support the hypothesis that fatty acid hydroperoxides accumulate in the arterial wall during atherosclerosis. On the other hand, the quantity of esterified 13-HODE and 15-HETE was increased markedly after exposure to molsidomine. The high dose of this agent could have initiated radical reactions (via liberation of NO and production of superoxide anions) thereby leading to a raise of the 13-HODE and 15-HETE content of the vessel.
 ...
PMID:Early atherosclerosis is accompanied by a decreased rather than an increased accumulation of fatty acid hydroxyderivatives. 165 Feb 7

Exogenous hypercholesterolemic (ExHC) rats, that develop hypercholesterolemia for exogenous cholesterol, are an established strain Isolated from Sprague-Dawley (SD) rats by Imai and Matsumura ((1973) Atherosclerosis, 18, 59-64). The present study was carried out to clarify the cause of hyperresponsivity in ExHC rats to dietary cholesterol. As early as one day after feeding a high cholesterol diet (1%) serum cholesterol level was doubled in ExHC rats, while the level of hepatic cholesterol was two-thirds of SD rats. The elevation of serum cholesterol was mainly attributed to the d less than 1.006 g/ml fractions. Cholesterol feeding increased fecal bile acid excretion in both strains, but to a more greater extent in SD rats. Absorption of dietary cholesterol and synthesis of cholesterol in vivo were similar between the strains. The uptake of beta-very-low-density-lipoproteins (beta-VLDL) in vivo and the primary cultured hepatocytes was lower in ExHC rats, when a high-cholesterol diet was fed. Even without feeding of a high-cholesterol diet, preincubation with cholesterol-rich lipoproteins caused a lower association and degradation of beta-VLDL by the hepatocytes from ExHC rats. Incubation of hepatocytes with cholesterol-rich lipoproteins did not affect the secretion of [14C]cholesterol into the density less than 1.006 g/ml fraction, but suppressed the secretion into the medium density greater than 1.006 g/ml fractions. These results suggest that ExHC rats, as compared to SD rats, are defective of hepatic uptake and processing cholesterol to bile acids.
 ...
PMID:Cholesterol metabolism in ExHC (exogenous hypercholesterolemic) rats. 173 41

Since its inception in 1983 the Canadian Atherosclerosis Society (CAS) has established itself firmly on the national and international scene as a forceful scientific voice. Its presence and activities have had their dominant expression at annual meetings held jointly with the Royal College of Physicians and Surgeons of Canada (RCPSC) and the Canadian Society for Clinical Investigation (CSCI) and in sponsoring other scientific and educational events, the most important of which was the Canadian Consensus Conference on Cholesterol (Ottawa, March 1988). It provided a forum for interaction between the scientific community, government, funding agencies, industry and the general public, and culminated in concrete recommendations for the populace of Canada. It also 'induced' a continuum in governmental and public concern for health with respect to atherosclerosis, and beyond it, the field of cardiovascular diseases. This dialogue continues. As a member (Constituent Society) of the International Atherosclerosis Society (IAS), the CAS has a voice in the international community, its policies and activities. The membership increase from 69 in 1983 to 175 in 1991 reflects steady growth of the CAS. The Society has been active in other areas (publications, awards for young investigators, and common educational endeavours with other groups) and will be host to the 1994 International Symposium on Atherosclerosis. Over a short period of only eight years, all of the above attests to sufficient progress (or achievement) for any scientific society. And yet, there remain quite a few areas not addressed as yet and some sad experiences (eg, that with the Long Term Planning Committee) that must be quickly remedied, if the Society is to keep pace with the everchanging emphasis in research that in the final analysis aims at improving the overall well-being and health of all Canadians. Inherent in the definition of history is the premise that accounts be provided of facts only. Historians who research their subjects derive these facts from studying the necessary accounts relating to these 'facts', using different and preferably controversial resources, so as to present the facts as objectively as possible. It is impossible, however, to fulfill all the above criteria for a historian who lived through every phase of 'life' of the subject of his or her account, because no matter how objective one wishes to remain (and bends backwards to achieve this) there will be always an element of a personal prism through which the historian lived the 'life' with his subject. For being human and thus unable to eliminate entirely that personal component, this writer asks humbly for the reader's understanding.
 ...
PMID:The Canadian Atherosclerosis Society--history and present status. 174 71

Cholesterol is converted to cholic acid and chenodeoxycholic acid by a series of reactions involving modifications to the steroid nucleus and oxidation of the side chain. These reactions can be affected by a number of inborn errors of metabolism. When this happens unusual bile acids or bile alcohols are synthesized; these can be identified using gas chromatography-mass spectrometry and fast atom bombardment mass spectrometry techniques. Two defects affecting the modifications to the steroid nucleus have been described; both present with cholestatic liver disease of neonatal onset. The better characterized of the two--3 beta-hydroxy-delta 5-C27-steroid dehydrogenase deficiency--leads to excretion of 3 beta-7 alpha-dihydroxy-5-cholenoic acid and 3 beta,7 alpha,12 alpha-trihydroxy-5-cholenoic acid in the urine. The liver disease improves dramatically on treatment with chenodeoxycholic acid. Deficient activity of 3-oxo-delta 4-steroid 5 beta-reductase is thought to be the cause of familial liver disease in some infants who excrete 7 alpha-hydroxy-3-oxo-4-cholenoic acid and 7 alpha,12 alpha-dihydroxy-3-oxo-4-cholenoic acid in the urine. However, diagnosis of this disorder is problematical; a similar pattern of metabolite excretion can occur as a result of liver damage caused by viruses or inborn errors of pathways unrelated to bile acid synthesis. Defective side chain oxidation in patients with cerebrotendinous xanthomatosis (CTX) leads to synthesis of bile alcohols such as 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25-tetrol and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,23,25-pentol. Patients with CTX do not have cholestatic liver disease. Their major problems (neurological disease, atherosclerosis and xanthomata) are caused by accumulation of cholestanol and cholesterol in the tissues. Bile acid precursors are probably diverted into synthesis of cholestanol. Chenodeoxycholic acid suppresses the production of abnormal metabolites from cholesterol (by inhibition of cholesterol 7 alpha-hydroxylase) and leads to improvement in the neurological disease. Defective side chain oxidation also occurs in peroxisomal disorders but this time it leads to accumulation of C27 bile acids such as 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid (trihydroxycoprostanic acid, THCA). This compound is readily detected in the bile and plasma of patients with defects of peroxisome biogenesis. In patients with defects of a single peroxisomal beta-oxidation enzyme (the 3-hydroxyacyl-CoA component of the bifunctional protein or the thiolase), the major C27 bile acid in bile may be 3 alpha,7 alpha,12 alpha,24-tetrahydroxy-5 beta-cholestanoic acid (varanic acid).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Inborn errors of bile acid metabolism. 174 14

Cholesterol oxidase (3 beta-hydroxy-steroid oxidase) catalyzes the oxidation of cholesterol to 4-cholesten-3 one and other oxidized cholesterol derivatives. The purpose of the present study was to investigate its effects on cultured vascular smooth muscle cells. Cultured rabbit aortic smooth muscle cells were morphologically altered after exposure to cholesterol oxidase in the presence of culture medium containing 10% fetal calf serum. If fetal calf serum was absent, cells were unaffected by the treatment. The extent of morphological change of the smooth muscle cells was dependent upon the time of exposure to the enzyme and the concentration of cholesterol oxidase employed. After moderate treatment with cholesterol oxidase, cells excluded trypan blue. Further, a specific mitochondrial marker DASPMI (dimethyl aminostyryl-methyl-pyridiniumiodine) which was used as a fluorescent index of cell viability, revealed that cell viability was unchanged after moderate cholesterol oxidase treatment. Nile red, a hydrophobic probe which selectively stains intracellular lipid droplets, was applied to detect the cellular lipid content after treatment with cholesterol oxidase. Cellular nile red fluorescence intensity increased linearly with the time and concentration of cholesterol oxidase treatment. These results demonstrate that cholesterol oxidase alters lipid deposition in the cell and changes cell morphology. The primary site of action of cholesterol oxidase appears to be independent of the cell membrane itself and instead is dependent upon the lipid content in the surrounding culture media. These changes occur prior to the cytotoxic effects of extensive oxidation. Because oxidized cholesterol may play an important role in the pathogenesis of atherosclerosis, our results have implications for intracellular accumulation of lipids in smooth muscle cells during the atherosclerotic lesion.
 ...
PMID:Effects of cholesterol oxidase on cultured vascular smooth muscle cells. 177 Sep 44


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