Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum was incubated in vitro with and without inhibition of lecithin:cholesterol acyltransferase (LCAT, EC 2.3.1.43). High density lipoprotein2 (HDL2) and high density lipoprotein3 (HDL3) were separated by zonal ultracentrifugation and analysed for lipid and apoprotein contents. The incubation of fresh sera resulted in a time-dependent decrease in HDL3 and an increase in HDL2. At the end of 24 h incubation HDL3 disappeared completely and the HDL2 peak had reached its maximum. The newly formed HDL2 was relatively enriched in total protein (apoprotein A-I, C-apoproteins) and cholesteryl esters, and depleted in phosphatidylcholine. Its migration in polyacrylamide gel electrophoresis was identical with HDL2 contained in fresh serum or HDL2 isolated from serum by zonal ultracentrifugation. The generated HDL2 particles exhibited the same electron microscopical characteristics as reference HDL2 samples prior to incubation. Addition of Ellman's reagent to the incubation mixture or heat inactivation of the samples prior to incubation resulted in a complete inhibition of HDL3/HDL2 interconversion, whereas addition of 1 mol/l NaCl had no detectable influence. There was also a substantial increase in HDL2 when VLDL-deficient serum was incubated at 37 degrees C. Similarly, in fresh serum from a patient affected with familial lipoprotein lipase deficiency, HDL3 was completely converted to HDL2. Our experiments demonstrate that LCAT promotes HDL3/HDL2 interconversion in native serum irrespective of the presence or absence of triglyceride-rich lipoproteins and lipoprotein lipase.
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PMID:The role of lecithin: cholesterol acyltransferase in high density lipoprotein3/high density lipoprotein2 interconversion. 706 21

Effects of 5-methyl-7-diethylamino-s-triazolo-1, 5-a) pyrimidine (trapidil, Rocornal), a therapeutic agent for ischemic heart disease, on various types of experimental hyperlipemias were studied. With administration of trapidil, elevation of serum high density lipoprotein cholesterol (HDL-C) levels and reduction in serum total cholesterol (TC), low density lipoprotein and very low density lipoprotein cholesterol (LDL-C) and the ratio of HDL-C to LDL-C (LDL-C/HDL-c) were observed in most disease models. Changes in HDL-C levels and LDL-C/HDL-C in the hyperlipemia induced by lipid-enriched diet in mice and in the hyperlipemia induced by high cholesterol diet in Japanese quails were of statistical significance. Also, amelioration of reduction in HDL-C induced by high fat emulsion plus 6-n-propyl-2-thiouracil in rats was observed to be significant. Moreover, trapidil significantly reduced TC, LDL-C levels and LDL-C/HDL-C in the hyperlipemia in hamsters. To investigate possible mechanisms of therapeutic effects of trapidil, blood enzyme activities in Japanese quails with hyperlipemia were assayed. Trapidil showed increases in plasma lipoprotein lipase and serum lecithin-cholesterol acyltransferase activities. These results suggest that trapidil may be an effective chemotherapeutic agent for treating ischemic heart disease.
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PMID:[Effects of 5-methyl-7-diethylamino-s-triazolo-(1, 5-a) pyrimidine (trapidil) on various experimental hyperlipemias (author's transl)]. 720 81

An experimental model was explored for the study of the effect of thyroid hormone on lipid transport and metabolism in the rat. The development of the hypothyroid state was accompanied by an early decrease in free fatty acids (FFA) followed by an increase in the level of cholesterol and a decrease in triglyceride concentration. Simultaneously, the adipose tissue lipoprotein lipase activity increased while the lecithin-cholesterol acyltransferase was unchanged. The hypothyroid state was also accompanied by a decrease in the concentrations of tryglycerides and cholesterol in very low density lipoproteins (VLDL) while the 2 lipids increased in the low density lipoprotein (LDL) fraction. Administration of triiodothyronine markedly reduced the amount of cholesterol in both the LDL and high density lipoprotein (HDL) fractions. The animal model has been shown to have similarities with findings in human subjects.
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PMID:Lipid transport in the hypothyroid rat as reflected by the serum concentrations of free fatty acids, lipoproteins, lecithin-cholesterol acyltransferase and lipoprotein lipase activity in adipose tissue. 724 Jun 72

In twenty-two men with "normal" findings clinically, by exercise ECG and laboratory tests, we performed an i.v. fat tolerance test, measurement of LCAT activity and the activities of post-heparin triglyceride lipases, and estimated serum lipids. HDL cholesterol was positively correlated to lipoprotein lipase (r=0.50, p < 0.05) and to the fractional removal rate of exogenous fat (r=0.59, p < 0.01), and negatively to the fasting levels of triglycerides (r=-0.65, p < 0.01). LCAT was neither correlated to HDL cholesterol nor to the fat removal rate. Our reseults confirm that a high triglyceride removal capacity is closely correlated to a high level of HDL. The association between the catabolism of triglyceride-rich lipoproteins and HDL was thus further substantiated.
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PMID:The relation between the levels of HDL cholesterol and the capacity for removal of triglycerides. 743 60

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.
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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

The possibility that risk of a atherosclerosis complication increases with oral contraceptive use was examined by studying the effect of oral pill containing 0.067 mg menstranol and 0.667 mg ehtynodiol diacetate/kg body weight on the metabolism of lipids in female rats fed a hypercholesterolemic diet for three months. Experimental group clearly exhibited higher levels of triglycerides and cholesterol in plasma and tissues, increase in aorta observed to be two folds. Increased hepatic cholesterogenesis was noted with treatment of oral contraceptive as indicated by higher activity of HMG-CoA reductase. Activity of lipoprotein lipase of extrahepatic tissue was depressed in experimental group. Activity of plasma LCAT, an enzyme involved in the transport of cholesterol from tissues, was also lower with treatment of oral contraceptive. However, activity of malic enzyme and glucose-6-phosphate dehydrogenase enhanced considerably with administration of oral pill. The increase in plasma and aortic cholesterol levels, increase in LDL+VLDL cholesterol and considerable decrease in HDL cholesterol in animals treated with oral contraceptives and fed with atherogenic diet, indicates that prolonged administration of oral pill may predispose towards atherosclerosis.
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PMID:Role of oral contraceptive in atherosclerosis. 792 21

Lipoproteins are circulating complexes of lipids and proteins, the transport and metabolism of which are directly controlled by apolipoproteins A-I, A-II, A-IV, B, C-I, C-II, C-III, D, E, and (a); lipoprotein-processing proteins lipoprotein lipase, hepatic lipase, lecithin-cholesterol acyltransferase, and cholesteryl ester-transfer protein; and lipoprotein receptors, low density lipoprotein (LDL) receptor, chylomicron remnant receptor, and scavenger receptors. Studies have shown a close association between lipoprotein abnormalities and coronary artery disease susceptibility. Four types of abnormalities are frequently seen: increased LDL cholesterol levels; decreased high density lipoprotein cholesterol levels, usually accompanied by increased triglyceride or very low density lipoprotein levels; increased concentrations of chylomicron remnants and intermediate density lipoproteins; and increased concentrations of an abnormal lipoprotein, lipoprotein (a). One or more of these abnormalities is present in 50-80% of myocardial infarction survivors. The exact pathogenic process whereby each of these abnormalities causes coronary artery disease is a subject of active investigation but beyond the scope of this brief presentation. However, the genetic contribution to each of these abnormal lipoprotein phenotypes is coming into focus and is discussed.
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PMID:Genetics of lipoprotein disorders. 846 76

Administration of nicotine to rats resulted in increased concentration of cholesterol, phospholipids and triglycerides in the serum and tissues. HDL cholesterol decreased while the LDL + VLDL cholesterol increased. There was increased tissue cholesterogenesis as evident from the increased activity of HMG-CoA reductase and increased incorporation into tissue unesterified cholesterol. Increased triglyceride synthesis in the tissues was evident from the increased activity of lipogenic enzymes and increased incorporation of label. Hepatic degradation of cholesterol to bile acids was decreased. The uptake of circulating triglyceride rich lipoproteins (chylomicrons and VLDL) was also decreased as revealed by the decreased activity of extrahepatic lipoprotein lipase. Plasma LCAT activity also showed a decrease in the rats given nicotine. The changes produced in the metabolism of lipids on nicotine administration were thus similar to those observed on exposure of rats to cigarette smoke, and it is felt that nicotine may therefore contribute at least partly to the risk posed by cigarette smoking in the development of atherosclerosis.
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PMID:Effect of nicotine administration on lipid metabolism in rats. 849 91

In eight patients with familial hypercholesterolemia the effects of two lipid reducing drugs on subpopulations of high density lipoproteins (HDL) were examined. After a 14-week period of diet and diet/placebo a 12-week therapy followed with either bezafibrate (CAS 41859-67-0) or fluvastatin (CAS 93957-55-2). Throughout both treatments a significant decrease of total and low density lipoprotein (LDL)-cholesterol, apolipoprotein B and triglycerides during both therapies were noted as well as an insignificant increase of HDL-cholesterol during bezafibrate. The nondenaturating gradient gel electrophoresis is a valid method for the investigation of the behaviour of HDL and was therefore chosen for this investigation. The individual HDL pattern and HDL diameters did not change in these subjects. The effect on the amounts of HDL 3b and HDL 3c was significantly more extensive during fluvastatin (+2.4% resp. + 2.9%) as compared to during bezafibrate therapy (+1.7% resp. + 2.9%). The changes noted in the HDL subclasses are probably due to a variable lipoprotein metabolism, for example increased activity of lipoprotein lipase, hepatic triglyceride lipase, lecithin-cholesterol acyltransferase and cholesterol ester transfer protein.
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PMID:Effect of fluvastatin or bezafibrate on the distribution of high density lipoprotein subpopulations in patients with familial hypercholesterolemia. 887 36

This paper provides a broad overview of biochemical risk factors such cholesterol and triglyceride in atherosclerotic cardiovascular diseases from the perspective of clinical laboratory medicine, since additional knowledge is needed in the genetic, biochemical, clinical and epidemiological spheres. Lipids play an important role in cell metabolism. Fatty acids and triglycerides, their storage form, are a high energy metabolic fuel. Cholesterol and phospholipids are essential components of cell membranes and cholesterol is a precursor of steroids. Cholesterol is delivered to the liver either from the intestine following dietary intake or is transported from extrahepatic tissues. It is removed from the liver through incorporation into lipoproteins by conversion into bile acids, and by secretion into bile. Lipoproteins are transported between tissues and organs in the form of particles. Lipoproteins are metabolically inert and apolipoproteins involve enzyme activation and inhibition of lipoprotein lipase, hepatic triglyceride lipase and lecithin-cholesterol acyltransferase. There is an exchange of components between lipoprotein particles facilitated by the cholesterol ester transfer protein. Lipoprotein receptors control the rate of cellular uptake and degradation and indirectly the rate of de novo cholesterol synthesis and individual subclasses of major lipoprotein species as well as the apolipoproteins and even the products of oxidative damage inflicted on the lipoprotein. This paper summarizes the relevant physiological and clinical knowledge and reviews a series of very practical data that must be understood to accurately quantify laboratory parameters.
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PMID:[Biochemistry of risk factors for cardiovascular diseases in laboratory medicine]. 895 35


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