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

Arteriosclerotic lesions were formed in rat aorta by the administration of vitamin D2, a high-fat diet and a thyroid suppressing agent. This treatment increased the serum total cholesterol level to 12 times the control level. In the arteriosclerotic lesions that were induced the activities of lysosomal enzymes, such as acid phosphatase and acid lipase, were higher than in controls, that of acid cholesterol esterase was decreased, those of microsomal lipid-synthesizing enzymes--such as acyl-CoA synthetase and cholesterol ester synthesizing activity--were increased and that of neutral cholesterol esterase was decreased. These data suggest that lipid metabolism in arteriosclerotic lesions was changed, resulting in the accumulation of cholesterol esters in the aorta. Administration of high-fat diet and thyroid suppressing agent also increased the serum cholesterol levels to 12-fold the control level, but did not induce arteriosclerotic lesions. After this treatment the activities of hydrolyzing enzymes, such as acid and neutral cholesterol esterase and lipase, in the aorta increased, but the activities of lipid synthesizing enzymes also increased. These data suggest that lipid metabolism in the aorta in this condition changed to compensate for the large influx of serum lipids and to prevent arteriosclerosis. The roles of the serum lipid level, cell injury and lipid metabolism in the aorta in forming arteriosclerotic lesions are discussed on the basis of these results.
Atherosclerosis 1982 May
PMID:Lipid metabolism in arteriosclerotic arterial wall of rats. 709 82

Sex differences in aortic cholesterol esterase activity and changes in the activity following castration and gonadal hormone treatment were investigated in rats. Differences in the enzyme activity were apparent after 2.5 months and became most significant after 6 months. The activity in the aorta and the liver was significantly higher in female rats. Prepubertal orchiectomy increased the aortic activity, feminizing the type of metabolism, whereas postpubertal orchiectomy, and both pre- and postpubertal ovariectomy induced no change in the activity. The administration of testosterone to female rats significantly decreased the aortic activity, masculinizing the type of metabolism. However, the administration of testosterone or of 17 beta-estradiol to male rats had no effect. These results suggest (1) that there are clear sex differences in aortic cholesterol esterase activity, (2) that prepubertal exposure to androgens plays a critical role in the sexual differentiation in aortic and hepatic cholesterol ester metabolism, and (3) that the administration of testosterone can temporarily masculinize the type of metabolism. These results partly explain the sexual differences in susceptibility to atherosclerosis.
Atherosclerosis 1982 Jun
PMID:Sex differences in aortic cholesterol esterase activity in rats, and changes of the activity following castration and gonadal hormone treatment. 711 69

The characteristics and properties of lipid metabolism in the aorta and the brain microvessels of rabbits were investigated to clarify the role of lipid metabolism in formation of atherosclerosis. In rabbit aorta, cholesterol esterase and lipase each had an acidic and a neutral optimum pH, whereas acyl-CoA synthetase, acyl-CoA: cholesterol acyltransferase, triglyceride synthesizing activity and choline phosphotransferase each had one neutral optimum pH. These pH optima were similar to those in rats. High cholesterol diet induced atheromatous lesions in the aorta, but not in the brain microvessels. In atheromatous aorta, the acid lipase and acid phosphatase activities were higher than in controls, but not the acid cholesterol esterase activity. Moreover the activities of neutral lipase, acyl-CoA synthetase, acyl-CoA:cholesterol acyltransferase, triglyceride synthesis and choline phosphotransferase were increased, but neutral cholesterol esterase activity was normal. These data suggest that lipis metabolism in the atheromatous aorta is changed in a manner favoring accumulation of lipids, especially cholesterol esters. In controls, most of the above enzyme activities in the brain microvessels were higher than those in the aorta. However, these enzyme activities in the brain microvessels were not changed by cholesterol feeding. Thus it is suggested that the properties of lipid metabolism in the aorta and brain microvessels, including permeability of lipoproteins into the vessel walls, are important in formation of atherosclerosis in addition to the serum factors.
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PMID:Lipid metabolism in the aorta and the brain microvessels of rabbits on high cholesterol diet. 718 94

In spontaneously hypertensive rats, prolonged hypertension caused a decrease in aortic cholesterol esterase activity with N-acetyl-beta-D-glucosaminidase activity increased and acid phosphatase activity unchanged [3]. The present study was undertaken to compare these changes with those caused by other experimentally induced types of hypertension. Treatment with DOCA-salt for one month significantly elevated both aortic cholesterol esterase and acid phosphatase activities. In contrast, to spontaneous hypertension, venous changes were also observed. An intake of 1% NaCl ad libitum produced results similar to those with the DOCA-salt treatment, despite the fact that blood pressure did not increase. This suggested that humoral factors were the main cause of the elevated enzyme activities in DOCA-salt hypertension. In rats made hypertensive by unilateral renal arterial constriction with contralateral nephrectomy (one clip--one kidney hypertension) or without contralateral nephrectomy (one clip--two kidney hypertension), aortic cholesterol esterase activities were unchanged, while aortic N-acetyl-beta-D-glucosaminidase, and aortic and venous acid phosphatase activities were increased. These results show distinct differences in the response of lysosomal enzymes during the three hypertensive states.
Atherosclerosis 1981 Jul
PMID:Aortic cholesterol esterase and other lysosomal enzyme activities in DOCA-salt, renal and spontaneous hypertension in the rat. 725 25

The total serum cholesterol level in rats fed on a high cholesterol diet (HCD) for 16 weeks was markedly higher than that in rats fed on a normal diet (ND), but pantethine reduced the increased level in rats fed on HCD (P less than 0.05). Acid cholesterol esterase activity (acid CEase) of arterial wall homogenates from rats fed on HCD was significantly lower than that of rats fed on ND (P less than 0.005). Acid CEase activity in the arterial wall of rats fed on HCD for 8 weeks and then ND for 8 weeks was less than that of rats fed on ND for 16 weeks. Acid CEase activity in the arterial wall was increased in rats fed on pantethine-containing diet. The ratio of cholesterol ester synthesizing activity to neutral cholesterol esterase (neutral CEase) activity was higher in rats fed on NCD than in those fed on ND. The ratio was lower in rats on the pantethine-containing diet than in those on NCD. The relationship between hypercholesterolemia and lipid metabolism in the arterial wall and effects of pantethine are discussed on the basis of these results.
Atherosclerosis 1980 May
PMID:Effect of pantethine on cholesterol ester metabolism in rat arterial wall. 738 78

Combined treatment with trypsin, cholesterol esterase, and neuraminidase transforms LDL, but not HDL or VLDL, to particles with properties akin to those of lipid extracted from atherosclerotic lesions. Single or double enzyme modifications, or treatment with phospholipase C, or simple vortexing are ineffective. Triple enzyme treatment disrupts the ordered and uniform structure of LDL particles, and gives rise to the formation of inhomogeneous lipid droplets 10-200 nm in diameter with a pronounced net negative charge, but lacking significant amounts of oxidized lipid. Enzymatically modified LDL (E-LDL), but not oxidatively modified LDL (ox-LDL), is endowed with potent complement-activating capacity. As previously found for lipid isolated from atherosclerotic lesions, complement activation occurs to completion via the alternative pathway and is independent of antibody. E-LDL is rapidly taken up by human macrophages to an extent exceeding the uptake of acetylated LDL (ac-LDL) or oxidatively modified LDL. After 16 h, cholesteryl oleate ester formation induced by E-LDL (50 micrograms/ml cholesterol) was in the range of 6-10 nmol/mg protein compared with 3-6 nmol/mg induced by an equivalent amount of acetylated LDL. At this concentration, E-LDL was essentially devoid of direct cytotoxic effects. Competition experiments indicated that uptake of E-LDL was mediated in part by ox-LDL receptor(s). Thus, approximately 90% of 125I-ox-LDL degradation was inhibited by a 2-fold excess of unlabeled E-LDL. Uptake of 125I-LDL was not inhibited by E-LDL. We hypothesize that extracellular enzymatic modification may represent an important step linking subendothelial deposition of LDL to the initiation of atherosclerosis.
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PMID:On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety. 750 42

Plasma cholesterol level is controlled by various factors. In the present study, high plasma activity of cholesterol esterase was found to correlate with plasma total cholesterol and low density lipoprotein (LDL) cholesterol levels in normolipidemic human subjects. However, the cholesterol esterase is not elevated in plasma of patients with familial hypercholesterolemia. These observations suggest that cholesterol esterase level is not determined by plasma cholesterol level, but elevated cholesterol esterase may be causative in increasing plasma cholesterol and LDL. Additional experiments further demonstrated that cholesterol esterase can convert the larger and less-atherogenic LDL to the smaller and more atherogenic LDL subspecies in vitro. These results suggest that plasma cholesterol esterase contributes to the formation and accumulation of atherogenic lipoproteins, and thus is a major risk factor for premature atherosclerosis in normal human subjects.
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PMID:Plasma cholesterol esterase level is a determinant for an atherogenic lipoprotein profile in normolipidemic human subjects. 754 36

Cholesterol metabolism in macrophages from atherosclerosis-prone C57BL/6J mice was compared with that in macrophages from atherosclerosis-resistant C3H/HeN mice. Plasma total cholesterol levels of both types of mice were significantly increased, but HDL cholesterol level was increased only in C3H/HeN mice when a high-cholesterol diet (1% cholesterol) was fed for 5 weeks. After incubation of macrophages from male and female mice on the high-cholesterol diet with beta-VLDL for 24 hours, cholesterol content in macrophages from C57BL/6J was approximately 1.5- to 2.0-fold higher than in those from C3H/HeN mice. [3H]Cholesterol oleate-beta-VLDL incorporation into macrophages from C57BL/6J mice on the high-cholesterol diet was greater than incorporation into those from C3H/HeN mice. The release of [3H]cholesterol from macrophages from C57BL/6J mice on the high-cholesterol diet was one seventh that from macrophages from C57BL/6J mice on the basal diet or that from macrophages from C3H/HeN mice on the basal or high-cholesterol diet. Acid cholesterol esterase activity was almost the same in macrophages from any group. Acyl CoA:cholesterol acyltransferase activity in macrophages from C57BL/6J mice on the high-cholesterol diet increased compared with that from macrophages from C57BL/6J mice on the normal diet. Neutral cholesterol esterase activity in macrophages from C57BL/6J mice was about half of that in macrophages from C3H/HeN mice independent of the type of diet. There were no sex differences in these metabolisms. Considered with our previous data, these results suggested that a high-cholesterol diet may cause metabolic changes to accumulate cholesterol ester in macrophages from C57BL/6J mice in accordance with genetic abnormalities.
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PMID:Genetic differences of lipid metabolism in macrophages from C57BL/6J and C3H/HeN mice. 762 13

Lipid testing has progressed from early measurements of total lipid by extraction and weighing to assess the fat content of the specimen. This nonspecific approach to lipid testing has been replaced in clinical laboratories by automated and quantitative procedures that avoid the extraction process. Instead, selective enzymes are utilized in reaction schemes to quantitate the individual lipid classes present in patient specimens. For example, cholesterol esterase and oxidase are used on a routine basis to measure total cholesterol in plasma and serum specimens. Similar use of other enzyme systems has permitted triglycerides and phospholipids to be measured by clinical laboratories. Lipid and lipoprotein measurements have advanced considerably from the early nonspecific extraction and gravimetric analysis schemes to the specific automated procedures that are commonly used today. However, as lipids and lipoproteins increased in their clinical usefulness as cardiovascular risk assessment tools, the search intensified for newer approaches to measure these entities more easily and more accurately. The influence of National Cholesterol Education Program has played a key role in highlighting the importance of lipids and lipoprotein analysis. Today, lipid testing is available outside the traditional laboratory environments - drugstores sell units that individuals can use at home to assess cholesterol levels. Lipid testing has come a long way, and we have only begun to experience some of the remarkable changes for the future.
Atherosclerosis 1994 Aug
PMID:Lipid testing for the year 2000 and beyond. 780 24

Several lipases and their cofactors are involved in the absorption, transport, storage, and mobilization of lipids. As part of an effort to examine the role of these enzymes in plasma lipid metabolism and genetic susceptibility to atherosclerosis, we report the chromosomal mapping of their genes in mouse. Restriction fragment length variants for each gene were identified, typed in an interspecific cross, and tested for linkage to known chromosomal markers. The gene for pancreatic lipase resides on chromosome 19, while the gene for its cofactor, colipase, is on chromosome 17. A gene for a protein with sequence similarity to pancreatic lipase was tightly linked (no observed recombination) to the gene for pancreatic lipase, suggesting a gene cluster. The gene for hormone-sensitive lipase is near the gene cluster containing apolipoproteins C-II and E on chromosome 7. The gene for hepatic lipase is near the gene for apolipoprotein A-I on chromosome 9. The carboxyl ester lipase gene resides on chromosome 2. Previously, we have mapped the gene for lipoprotein lipase to chromosome 8. Thus, with the exception of pancreatic lipase and a related protein, these lipase genes, including several that are members of a gene family, are widely dispersed in the genome. Comparison of chromosomal locations for these genes in mouse and humans shows that the previously observed interspecies syntenies are preserved.
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PMID:Chromosomal localization of lipolytic enzymes in the mouse: pancreatic lipase, colipase, hormone-sensitive lipase, hepatic lipase, and carboxyl ester lipase. 810 16


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