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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

It is generally accepted that the cell population of naturally occurring and experimental atherosclerotic lesions is constituted by smooth muscle cells and non-myogenic foam cells of monocytic origin. In the present investigation we studied aortic fatty streaks from cholesterol-fed African green monkeys. In addition to the traditionally recognized cell types, the majority of the lesions examined contained intimal granulocytic cells identified by their ultrastructural characteristics and granular content as neutrophils, mast cells-basophils, and eosinophils. The neutrophils, and mast cells-basophils additionally contained numerous cytoplasmic lipid droplets. The consistent observation of these cell types in our material suggests that these granulocytic elements are part of the cell population of fatty streaks. The role of these cells is not clear as yet, but it is likely that the enzymatic activity of neutrophils such as lipase, phospholipases A and B, elastase and collagenase may play a role in the clearing of arterial lipid as well as in arterial wall remodeling. The content and release of heparin and histamine by basophils and mast cells may play a role in preventing thrombus formation and in promoting lipolysis. Eosinophil peroxidase may activate histamine release by basophils and mast cells. The cytoplasmic lipid accumulation by neutrophils, basophils and mast cells may in turn contribute to the population of foam cells in these lesions.
Atherosclerosis 1982 Jun
PMID:The cell population of aortic fatty streaks in African green monkeys with special reference to granulocytic cells. An ultrastructural study. 711 63

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

The paper discusses changes in the activity of lipolytic enzymes in blood plasma of rats before and after heparin administration in the course of experimental atherosclerosis development. This development was shown to be characterized by an abrupt rise of preheparin plasma level (comparatively to normal) and of monoacylglycerolipase and tributyrinase activity, with this rise being unchanged throughout the experiment. An increase in the postheparin plasma activity of heparin-dependent lipolytic enzymes, lipoprotein lipase, triacylglycerolipase, monoacylglycerolipase, and tributyrinase was seen only in the initial stage of the disease. After 30-40 weeks the activity of the enzymes was below normal. It is concluded that the increased activity of lipoproteid lipase and triacylglycerolipase is related to their activation in the blood channel.
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PMID:[Changes in the lipolytic enzymatic activity of the blood in rats maintained on an atherogenic diet]. 726 45

The postheparin plasma lipoprotein lipase (LPL) activity and plasma HDL and LDL cholesterol concentrations, decreases significantly during probucol treatment of the rat. The reduction of the LPL activity obviously took place in adipose tissue. The activity of hepatic lipase and the in vitro synthesis of cholesterol in the liver or isolated jejunal villous cells were unaffected by the probucol treatment. Plasma triglyceride and VLDL cholesterol concentrations remained similar in the control and probucol groups despite the difference in the LPL activity, whereas the esterified VLDL cholesterol level was significantly reduced in the probucol group. The results suggest that the HDL lowering action of probucol is contributed by the reduced LPL activity probably via impaired VLDL metabolism.
Atherosclerosis
PMID:Effect of probucol on cholesterol synthesis, plasma lipoproteins and the activities of lipoprotein and hepatic lipase in the rat. 733

Previous animal studies have shown that the heparin-releasable hepatic lipase (HL) is located on the luminal surface of the liver endothelial cells and may have a function in the removal of high density lipoprotein lipids from plasma. We therefore examined the relationship between plasma HDL levels and the HL activity of postheparin plasma in a group of young, very fit men who were living under strictly controlled comparable conditions (military academy studients). HDL2 cholesterol, HDL2 phospholipid and HDL2 protein concentrations each showed a highly significant negative correlation with postheparin HL activity. A similar but slightly lower inverse relationship was also present between total HDL lipids and HL activity, whereas no correlation could be observed between any of the HDL3 lipids and HL activity. The cholesterol/protein ratio of HDL2 correlated negatively with the HL activity. These results support the hypothesis that the hepatic endothelial lipase has a physiological role in the degradation and removal of circulating HDL2.
Atherosclerosis 1980 Aug
PMID:Evidence for the role of hepatic endothelial lipase in the metabolism of plasma high density lipoprotein2 in man. 741 75

Post-heparin lipoprotein lipase (PH-LPL)-high density lipoprotein cholesterol (HDL-C) interrrelationships were assessed in 9 subjects with documented familial hyperalphalipoproteinemia (FHA) and in 8 controls to focus on potential biochemical etiologies of FHA and relationships of HDL-C to triglyceride hydrolysis and PH-LPL. FHA subjects had mean HDL-C and HDL2-C levels > twice controls; their PH-LPL levels (mean +/- SEM) (3.14 +/- 2.3 mumol FFA/h/ml) were also > twice that of controls (15.0 +/- 1.6) (P < 0.01), but post-heparin hepatic lipase levels (PH-HL) in the FHA and control subjects did not differ (18.1 +/- 1.6 vs 26.6 +/- 4.3, P > 0.1). For all subjects (FHA and controls) PH-LPL was positively correlated with HDL-C (r = 0.79, P < 0.01) and with HDL2-C (r = 0.90, P < 0.01), but not with HDL3-C (r = --0.02). There were no significant PH-HL and HDL-C interrelationships, P > 0.1. The amount of apo CII (the primary activator of PH-LPL) in HDL2 was greater in the FHA (mean +/- SEM) (16.1 +/- 2.5 microgram/ml plasma) than in control subjects (4.7 +/- 0.9, P < 0.01). There were strong positive correlations between HDL2 apo CII and both PH-LPL (r = 0.79, P < 0.01) and HDL2-C (r = 0.80, P < 0.01). Apo CII as a percentage of HDL2 protein was higher in FHA than control subjects (mean +/- SEM) (1.2 +/- 0.3% vs 0.5 +/- 0.2%, P < 0.01). Apo CII as a percentage of HDL3 protein was similar in FHA and control subjects. We postulate that increased turnover rate of triglyceride-rich lipoproteins due to high LPL activity may be an important factor leading to the elevation of HDL-C in FHA. The highly significant positive correlation between HDL2-C and PH-LPL provides strong clinical evidence for the theory that HDL2 is formed during the hydrolysis of triglycceride-rich lipoproteins. The high concentration of HDL2 apo CII in FHA subjects may be caused by increased catabolism of triglyceride-rich lipoproteins in the presence of high endothelial LPL, with transfer of apo CII from very low to high density lipoproteins.
Atherosclerosis 1980 Oct
PMID:Post-heparin plasma lipoprotein and hepatic lipases. Relationships to high density lipoprotein cholesterol and to apolipoprotein CII in familial hyperalphalipoproteinemic and in normal subjects. 742 98

Reverse cholesterol transport from peripheral tissues, including the arterial wall, involves high density lipoprotein (HDL) uptake of unesterified cell cholesterol, its esterification by lecithin-cholesterol-acyl-transferase (LCAT), direct HDL-cholesteryl ester uptake by the liver and the indirect pathway consisting of the cholesteryl ester transfer protein (CETP)-mediated transfer of HDL-cholesteryl ester to apolipoprotein (apo) B-containing lipoproteins (very low density lipoprotein (VLDL) and LDL). Although the first route should be regarded as anti-atherogenic, ambiguous interpretations are drawn from the indirect pathway since it is potentially atherogenic to the extent that it may raise the plasma cholesteryl ester concentration in lipoproteins that are taken up by arterial wall macrophages. In addition, controversial roles are played in reverse cholesterol transport by LCAT and liver uptake of HDL-cholesteryl ester mediated by hepatic lipase (HL). HDL may exert several antiatherogenic effects unrelated to its role in cell cholesterol removal.
Atherosclerosis 1995 Jul
PMID:Is reverse cholesterol transport a misnomer for suggesting its role in the prevention of atheroma formation? 748 24

We have studied low density lipoprotein (LDL) subclass distribution in a group of male patients with non-insulin-dependent diabetes mellitus (NIDDM) and investigated its relationships to fasting and postprandial triglyceride (TG)-rich lipoproteins, insulin resistance, lipoprotein lipase (EC 3.1.1.3; LPL), hepatic lipase (EC 3.1.1.34; HL), lecithin:cholesterol acyl transferase (EC 2.3.1.43; LCAT) and cholesteryl ester transfer protein (CETP) activities. LDL was subfractionated by density gradient ultracentrifugation. Postprandial lipoproteins were measured after an oral fat load using retinyl palmitate as a marker for intestinal TG-rich lipoproteins. Hypertriglyceridaemic NIDDMs (HTG) had a preponderance of small dense LDL particles present in the plasma and reduced amounts of large buoyant species when compared to normotriglyceridaemic patients (NTG) and controls. Both groups of diabetics were more insulin resistant than the controls (P < 0.05) and had raised concentrations of proinsulin (P < 0.05), although insulin content did not differ significantly. 32-33 split proinsulin (SPI) was the major insulin-like molecule present in HTG and was present in significantly higher amounts in these patients (P < 0.05) than either NTG or control subjects and correlated significantly with the presence of small dense LDL particles. After a test meal, the postprandial chylomicron response was greater in HTG than either NTG diabetics or controls (P < 0.05). Chylomicron remnants were present to a greater extent in HTG than in NTG and controls (P < 0.05), although in this case NTG also contained more chylomicron remnants than control subjects (P < 0.05). There was no difference in the LPL activity, CETP and LCAT between diabetics and controls, whereas an increase in hepatic lipase activity was seen in the HTG diabetics (P < 0.05). Both CETP and LCAT activities increased postprandially. Multivariate analysis showed that TG, HDL content and HL activity were the most important determinants of small dense LDL concentration in the fasting state (R2 = 67%). Postprandially, chylomicron remnant clearance, HL and insulin resistance were the major determinants (R2 = 61%) of LDL-III.
Atherosclerosis 1995 Mar
PMID:Fasting and postprandial determinants for the occurrence of small dense LDL species in non-insulin-dependent diabetic patients with and without hypertriglyceridaemia: the involvement of insulin, insulin precursor species and insulin resistance. 760 66

We present a 3 year follow up of a new type of hyperalphalipoproteinemia with stable high density lipoprotein (HDL) concentrations around 6.0 mmol/l in a female with persistently elevated erythrocyte sedimentation rate (ESR). By density gradient ultracentrifugation, next to the intensively colored HDL2-fraction, an additional band between HDL3 and the serum proteins was seen consistently. The patient's plasma contained an unique complex of albumin with apoprotein A-I. Her IgM was 3- to 4-fold elevated was not complexed to HDL. Familial forms of hyperalphalipoproteinemia could be excluded. As a presumed reason for the existence of the HDL-albumin complex we found that the patient's post-heparin plasma lipoprotein lipase activity was over 2-fold increased, while that of hepatic lipase was over 2-fold decreased: no common cause for the existence of the albumin complex and the increased concentration of IgM was found.
Atherosclerosis 1994 Nov
PMID:A case of hyperalphalipoproteinemia associated with albumin complexing. 784 Aug 9


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