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)

Human heart lipoprotein lipase was purified by affinity chromatography on heparin-Sepharose 4B. When crude extracts of heart acetone powder were applied to columsn, about 40% of total lipase activity was bound to the gel and then eluted with 1.5 M NaCl. At this stage the eluted enzyme was purified 1900-fold. Disc gel electrophoresis yielded a single protein band corresponding with lipolytic activity. Minimum molecular weight of the protein was 60,000 as determined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The purified enzyme was highly unstable; however, its activity could be partially stabilized at --20C by bovine serum albumin, glycerol, or ethylene glycol. The activity of the purified enzyme (i) had a pH optimum between 7.8 and 8.0; (ii) required serum for full enzymatic activity; apoC-II could be substituted for serum; (iii) was inhibited by by apoC-I in the presence of activated substrate; (iv) was markedly inhibited by NaCl; and (v) was stimulated by heparin.
Atherosclerosis
PMID:Purification and characterization of lipoprotein lipase from human heart. 0 61

The changes in the individual glycosaminoglycans of the aorta and in lipoprotein lipase activity of the aorta, liver and heart have been studied at various stages in the development of mild atheroma in the rat. Three responses were seen: (a) Hyaluronic acid initially decreased, then increased; (b) Heparan sulphate and chondroitin sulphates A and C initially increased, then decreased. (c) Chondroitin sulphate-B and heparin increased with progressing lipid infiltration and decreased markedly only in the later stages. Ageing changes were also investigated in the rat aorta: total cholesterol, phospholipids and triglycerides increased progressively from weaning to 9 months of age. Hyaluronic acid decreased after weaning, reached a minimum at 6 months and then increased thereafter. Heparan sulphate and chondroitin sulphate-C reached a maximum at 6 months and then decreased thereafter. Chondroitin sulphates A and B showed a similar but less marked pattern of change with age. Heparin progressively increased with age. Aortic lipoprotein lipase activity increased in the early stages of atheroma and then decreased as the lipid infiltration became more severe. The ageing study showed that enzyme activity was quite high at weaning. decreased considerably at 3 months, but thereafter fell only slightly.
Atherosclerosis
PMID:Changes in aortic glycosaminoglycans and lipoprotein lipase activity in rats with age and atheroma. 12 74

The very low density lipoproteins (VLDL) of fasting serum from subjects with normo- and hypertriglyceridaemia (Type IV and V) were separated into subfractions by density gradient centrifugation. The tetramethylurea (TMU)- soluble apolipoproteins were separated by polyacrylamide gel electrophoresis and the relative proportions of apo CII and CIIIs determined. There were highly significant correlations between the concentration of VLDL triglycerides and apo CII (r---0.92), apo CIII1 (r=+0.88) and the ratio apo CII/apo CIII1 (r= --0.94). It was suggested that the decreasing ratio apo CII/CIII1 with increasing triglyceride levels might cause a resistance to lipoprotein lipase and therefore a defect lipolysis of VLDL based upon a changed ratio apo CII/apo CII1 might be part of the pathogenesis of the hypertriglyceridaemia.
Atherosclerosis
PMID:Changing relative proportions of apolipoproteins CII and CIII of very low density lipoproteins in hypertriglyceridaemia. 17 29

The hydrolysis of an emulsified triglyceride substrate by clearing factor lipase (lipoprotein lipase) normally requires the presence of particular activating polypeptide species. These are present in serum, together with other inhibitory species, as part of the serum lipoproteins. The paper describes a method whereby the net activating ability of individual human sera may be measured routinely. In a normal population, this activating ability is shown to be correlated positively with the fasting serum triglyceride concentration. As the fasting triglyceride concentration increases, there is a rise in the proportion of the total activating ability that is associated with the very low density lipoproteins. A dietary fat load does not raise the total activating ability but does increase the proportion of the total that is associated with the serum lipoproteins of lowest density.
Atherosclerosis 1976 Sep
PMID:Clearing factor lipase (lipoprotein lipase) activator. A method for the measurement of the net activating ability of human sera. 18 2

Hypertriglyceridemia, a risk factor for premature atherosclerosis, may result from decreased use of plasma triglycerides by tissues. The removal of triglycerides is mediated by the enzyme lipoprotein lipase (LPL). Heparin releases LPL from tissues and post-heparin plasma lipolytic activity (PHLA) has been extensively used to elucidate the mechanism of hypertriglyceridemia in various diseases. There is evidence to show that postheparin plasma contains enzymes other than LPL. Hence data on total PHLA are difficult to interpret. Availability of assays for the LPL component of PHLA has clarified equivocal findings in certain hypertriglyceridemic states. However, the LPL component is also heterogeneous. The LPL "isoenzymes" from various extrahepatic tissues behave differently under various metabolic conditions. Therefore, to understand properly the LPL system it is necessary to study the specific tissue LPL. Furthermore, the serum activator for LPL is now characterized. Its importance is evidenced by the recent discovery of a hypertriglyceridemic patient deficient in this apoprotein.
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PMID:The lipoprotein lipase system: new understandings. 20 4

In vitro experiments showed that blood sera of the patients with atherosclerosis contained rather often the fraction of very low density lipoproteins (VLDL) with sf 100-400 S, which were cleaved by the lipoprotein lipase at the decreased rate as compared with that of normal people. The decrease in cleavage of the VLDL fraction was usually observed in patients with the increased concentration of the lipoprotein fraction in blood sera. These data suggest that separate constituents occurring in the VLDL fraction (sf 100-400 S) may be nonuniformly increased in hyperlipoproteinemia.
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PMID:[Lipoprotein lipase fractionation of very low density serum lipoproteins from healthy subjects and persons afflicted with atherosclerosis]. 21 May 86

We determined serum high-density lipoprotein cholesterol content and analyzed the approtein structure of the various lipoprotein fractions in 21 patients on chronic hemodialysis. High-density lipoprotein cholesterol was significantly reduced in all patients as compared with 11 normal persons (mean +/-1 standard deviation: 26 +/- 13 vs. 52 +/- 9 mg per 100 ml; P less than 0.001) whether or not triglyceride levels were raised. In seven of those with Type IV hyperlipoproteinemia, protein content of high-density lipoprotein and its subfractions 1, 2 and 3 were also reduced (P less than 0.001) in parallel with reductions in cholesterol in these fractions. Apoprotein electrophoresis showed an increase in "arginine-rich" peptide in very-low-density lipoprotein and high-density lipoprotein fraction 1, and a reduction in apoprotein Cll in very-low-density and high-density lipoprotein. In addition to their reduced high-density lipoprotein cholesterol levels, a major factor in the atherosclerosis of these patients may be their abnormal high-density lipoprotein composition. Their raised triglyceride levels could be due to defective lipoprotein lipase activation by the reduced very-low-density lipoprotein apoprotein.
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PMID:Defective high-density lipoprotein composition in patients on chronic hemodialysis. A possible mechanism for accelerated atherosclerosis. 21 15

Heparin-releasable lipoprotein lipase (LPL) activity was measured in biopsy samples of adipose tissue and skeletal muscle of 8 normal healthy females, first during an isocaloric diet and then after 2 and 7 days on a 400-kcal diet. In adipose tissue the LPL activity expressed per tissue weight fell to 38% and to 22% of the initial level after 2 and 7 days' caloric restriction, respectively. In skeletal muscle the LPL activity rose slightly after two days (+24%) but decreased to 49% of the initial value after seven days on diet. The estimated total body LPL activity decreased to 50% and to 20% of the baseline value after 2 and 7 days, respectively, but the relative contribution of skeletal muscle to the total LPL increased from 10 to 30%. The triglyceride and VLDL triglyceride concentrations were not significantly changed during the low calorie diet but the LDL triglyceride increased and the HDL cholesterol decreased significantly (P less than 0.01). It is concluded that substantial restriction of calorie intake results in a decrease of over-all triglyceride removal capacity but in an increase of the fraction removed by skeletal muscle. The decrease of HDL cholesterol is probably a consequence of the low turnover of exogenous and endogenous triglyceride-rich lipoproteins.
Atherosclerosis 1979 Mar
PMID:Effects of caloric restriction on lipid metabolism in man: changes of tissue lipoprotein lipase activities and of serum lipoproteins. 22 89

The anomalous finding that very low density lipoprotein levels are relatively normal in patients with familial hyperchylomicronaemia has never been satisfactorily explained, particularly in view of the marked reduction or absence of peripheral lipoprotein lipase activity characteristic of this condition. I propose that the discrepancy between the plasma levels of the two triglyceride-rich lipoprotein fractions in these patients is due to the secretion by the liver of triglyceride in the form of chylomicron-like particles, rather than as very low density lipoprotein. The proposed "switch" in the spectrum of lipoproteins secreted by the liver is probably contingent upon the activity of the hepatic lipase present on the liver cell plasma membrane.
Atherosclerosis 1979 Sep
PMID:Why very low density lipoprotein levels are normal in familial hyperchylomicronaemia. 22 32

Phthalazinol (EG 626), a thromboxane A2 antagonist and cyclic AMP phosphodiesterase inhibitor, has been shown to prevent the atherosclerosis induced in cholesterol fed rabbits. In an attempt to clarify the antiatherosclerotic mechanism, the effects of this compound on the lipolytic enzyme activities (cholesterol esterase and lipoprotein lipase) of rat aorta were examined in vivo. Administration of EG 626 (100-200 mg/kg, per os, daily, 1-2 weeks) affected neither the aortic lysosomal cholesterol esterase nor the acid phosphatase activity, whereas the lipoprotein lipase activity was signficantly decreased by the treatment. These results suggest that with an elevation in HDL-cholesterol, a decrease in lipoprotein lipase activity after ingestion of EG 626 might contribute, at least to some extent, to the prevention of arterial lipid accumulation.
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PMID:Effects of phthalazinol (EG 626) on arterial lipolytic enzyme activities in the rat. 23 31


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