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)

Small (Sf 20-100) very low density lipoprotein (VLDL) particles were prepared by density gradient ultracentrifugation of plasma from normolipidemic and type IV hypertriglyceridemic post-infarction patients and healthy controls. The small VLDL separated from the plasma of severely hypertriglyceridemic post-infarction patients were found to contain twice the amount of cholesteryl esters per particle, compared with small VLDL from normolipidemic patients and healthy controls. There was a linear increase in the percentage of cholesterol that was esterified in the small VLDL with the serum VLDL triglyceride concentration (r = 0.66). When incubated for two hours with bovine lipoprotein lipase in excess and bovine albumin as a free fatty acid acceptor at one and the same triglyceride concentration in the medium, the end-product isolated by ultracentrifugation varied as a function of the serum VLDL triglyceride level. The amount of glyceride-glycerol recovered after two hours of incubation with lipoprotein lipase was 13.3 +/- 1.3% (mean +/- SEM) of the initial values and did not correlate with the VLDL triglyceride level. With rising serum VLDL triglyceride concentration, the product isolated in the low density lipoprotein (LDL) density region (1.006 less than d less than 1.063 kg/l) contained more total cholesterol and phospholipids. The linear correlation coefficients for these relations were 0.65 and 0.58 for cholesterol and phospholipids respectively. The ratio of total cholesterol to insoluble protein in the LDL density range after lipolysis rose with increasing serum VLDL triglyceride level (r = 0.68). The end-product was further characterized by density gradient ultracentrifugation of the incubate. In vitro LDL derived by lipolysis of normolipidemic small VLDL was denser than in vitro LDL of hypertriglyceridemic small VLDL. A significant relation was found between the percentage of cholesteryl esters of total cholesterol in the substrate and the relative amount of total cholesterol recovered in the LDL density fraction after lipolysis (r = 0.69). We suggest that the enrichment with cholesteryl esters of small VLDL from type IV hypertriglyceridemic patients is caused by lipid transfer from LDL and high density lipoprotein (HDL) and that the change in VLDL particle composition influences the precursor-product relationship to LDL.
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PMID:Abnormalities of composition and of in vitro lipolysis products of human small very low density lipoproteins in hypertriglyceridemia. 236 Sep 14

Insects transport lipid for flight in the form of diacylglycerol-rich low density lipoproteins (low density lipophorin (LDLp)). A hybrid LDLp has been produced in vitro by using Locusta migratoria fat body, locust high density lipophorin, locust adipokinetic hormone, and Manduca sexta apolipophorin III (apoLp-III). The hybrid is similar in size and density to locust LDLp, contains several molecules of M. sexta apoLp-III, and lacks locust apoLp-III, as shown by immunochemical methods. Under the same conditions an apoLp-III from Thasus acutangulus is poorly incorporated into the locust lipoprotein. The role of apoLp-III as a recognition signal/activator of flight muscle lipoprotein lipase was assayed with labeled hybrid LDLp produced in vitro using M. sexta apoLp-III radiolabeled with 35S. In addition, hydrolysis of diacylglycerol was determined with lipid-labeled hybrid LDLp produced in vitro using [U-14C]glycerol incorporated into the diacylglycerol moiety. In vitro incubations of the labeled hybrid LDLp with L. migratoria flight muscles show that the lipase efficiently utilizes hybrid LDLp as a substrate and demonstrate that the carbohydrate moiety of locust apoLp-III (which is lacking in the M. sexta protein) is not required for interaction with the lipase. It also suggests that specific antigenic determinants of L. migratoria apoLp-III are not required for lipase activation since M. sexta apoLp-III lacks immunological cross-reactivity with L. migratoria apoLp-III.
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PMID:An insect lipoprotein hybrid helps to define the role of apolipophorin III. 244 3

The influence of training on fatty acid and glyceride synthesis by liver and adipose tissue homogenates of young and old Fischer-344 rats was examined. Four groups of rats (10 animals/group) were studied: young untrained, young trained, old untrained, and old trained. Training of each group was for 10 wk at 75% maximal O2 uptake. Young rats were killed at 6 mo of age and old rats were killed at 27 mo of age. Fatty acid synthesis was assessed by measuring the activities of acetyl-CoA carboxylase, fatty acid synthase, ATP citrate-lyase, "malic" enzyme, and glucose-6-phosphate dehydrogenase. Glyceride synthesis was evaluated by determining the rate of incorporation of [14C]glycerol 3-phosphate into lipids. In addition, lipoprotein lipase activity was measured in acetone-ether powders of adipose tissue from the four groups of rats. In liver, training had no effect on fatty acid or glyceride synthesis in either group. However, aging caused a significant decrease in the activities of four of the lipogenic enzymes but had no effect on glyceride synthesis. Training caused an increase in fatty acid synthase and glyceride synthesis in adipose tissue, and aging decreased lipoprotein lipase activity. It was concluded that training enhances the synthetic capacity of lipids by adipose tissue but that aging had a more profound effect in that the activities of the enzymes involved in these processes were lower in the old rats. Furthermore, the decreased activity of lipoprotein lipase in the older rats may explain the higher plasma triglyceride levels that were observed in these animals.
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PMID:Influence of age and exercise training on lipid metabolism in Fischer-344 rats. 257 7

In 87 patients (74 males, 13 females; age 43 +/- 9.2 years) covering a wide range of triglyceride (TG) concentrations (8.8 to 80.7 mmol/l) the turnover of total serum TG has been measured using the technique of labelling endogenously synthesized TG with 3H-glycerol. In parallel, lipoprotein lipase activity in adipose tissue and the adipose-tissue lipase activity in post-heparin plasma have been assessed following an oral 50 g glucose load. Despite the well-recognized function of this enzyme for intravascular lipolysis no direct relationship between lipase activities and fractional catabolic rates (FCR), reflecting TG removal processes, was found. On the other hand, relative enzyme activities (per TG moles) are positively correlated with the FCR. However, a detailed analysis of this relationship revealed that only in HTG patients whose FCR are below 0.210 h-1 a rate-limiting influence of a relative lipase deficit can be shown. In these patients, a statistically significant elevation of concentrations of free fatty acids is supposed to contribute to the impairment of the TG removal.
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PMID:Pathogenetic role of adipose tissue lipase deficit for development of hypertriglyceridaemia. 259 17

Fatty acids, the preferred substrate in normoxic myocardium, are derived from either exogenous or endogenous triacylglycerols. The supply of exogenous fatty acids is dependent of the rate of lipolysis in adipose tissue and of the lipoprotein lipase activity at the coronary vascular endothelium. A large part of the liberated fatty acids is reesterified with glycerol-3-phosphate and converted to triacylglycerols. Endogenous lipolysis and lipogenesis are intracellular compartmentalized multienzyme processes of which individual hormone-sensitive steps have been demonstrated in adipose tissue. The triacylglycerol lipase is the rate-limiting enzyme of lipolysis and glycerol-3-phosphate acyltransferase and possibly phosphatidate phosphohydrolase are the rate-limiting enzymes of lipogenesis. The hormonal regulation of both processes in heart is still a matter of dispute. Triacylglycerol lipase activity in myocardial tissue has two intracellular sources: 1. the endoplasmic reticular and soluble neutral lipase, and 2. the lysosomal acid lipase. Studies in our laboratory have indicated that whereas lipolysis is enhanced during global ischemia and anoxia, overall lipolytic enzyme activities in heart homogenates were not altered. In addition we were unable to demonstrate alterations in tissue triacylglycerol content and glycerol-3-phosphate acyltransferase activity under these conditions. Lipolysis, is subject to feedback inhibition by product fatty acids. Therefore all processes leading to an increased removal of fatty acids from the catalytic site of the lipase will stimulate lipolysis. These studies will be reviewed. In addition, studies from our department have demonstrated the capacity of myocardial lysosomes to take up and degrade added triacylglycerol-particles in vitro. Such a process, stimulated by Ca2+ and stimulated by acidosis, offers another physiological target for hormone actions.
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PMID:Hormones and triacylglycerol metabolism under normoxic and ischemic conditions. 267 63

Lipid emulsions were prepared with compositions similar to the triacylglycerol-rich plasma lipoproteins, but also incorporating added small amounts of monoacylglycerols. Control emulsions without monoacylglycerol were metabolized similarly to natural chylomicrons or very-low-density lipoproteins when injected intravenously in rats. The emulsion triacylglycerols and cholesteryl esters were both removed rapidly from the bloodstream, with the removal rates of triacylglycerols faster than those of cholesteryl esters. Much of the removed cholesteryl ester was found in the liver, but only a small fraction of the triacylglycerol, consistent with hepatic uptake of the triacylglycerol-depleted remnants of the injected emulsion. Emulsions incorporating added monooleoylglycerol or stearic acid were metabolized similarly. Added 1- or 2-monostearoylglycerol had no effect on triacylglycerol removal from plasma, but the removal rate of cholesteryl esters was decreased and less cholesteryl ester was found in the liver. These effects are similar to those recently described when emulsions and chylomicrons contained triacylglycerols with a saturated acyl chain at the glycerol 2-position, suggesting that saturated monoacylglycerol produced by the action of lipoprotein lipase may cause triacylglycerol-depleted remnant particles to remain in the plasma instead of being rapidly taken up by the liver.
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PMID:The effect of added monoacylglycerols on the removal from plasma of chylomicron-like emulsions injected intravenously in rats. 271 86

The administration of a single injection of tumor necrosis factor (TNF) produces a variety of acute and sustained biological effects, including hyperlipidemia, stimulation of hepatic lipogenesis, decreases in adipose tissue lipoprotein lipase activity, and anorexia with weight loss. Chronic administration of a fixed dose of TNF produces tachyphylaxis to the anorectic/cachectic effects of TNF. We now report that the hyperlipidemic effect of TNF persists during chronic TNF administration in the absence of any cachectic effect of TNF. Sprague-Dawley rats injected with TNF (250 micrograms/kg) show a significant decrease in weight over the next 24 h which can be accounted for by decreases in food and water intake accompanied by an increase in urine output. With subsequent daily injections of TNF, treated rats begin eating and rapidly regain weight. Hypertriglyceridemia persists for up to 10 days of daily injections of TNF. After three daily injections of TNF, no decreases were seen in lipoprotein lipase activity in a wide variety of tissues. De novo hepatic lipogenesis remained increased in TNF-treated animals after four daily injections, but by the fifth day hepatic lipogenesis returned to normal. After 5 days of TNF treatment the acute incorporation of labeled glycerol into serum triglycerides remained elevated. These data indicate that hyperlipidemia persists during multiple daily injections of TNF and that TNF induced hypertriglyceridemia is not inevitably linked to the syndrome of cachexia.
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PMID:Persistence of the hypertriglyceridemic effect of tumor necrosis factor despite development of tachyphylaxis to its anorectic/cachectic effects in rats. 271 42

Prolonged parenteral nutrition frequently includes lipid emulsions. This report investigates how emulsions containing triacylglycerols of different molecular weight affect the rate of clearance in vivo and the activity in vitro of the two enzymes responsible for this clearance: diaphragm lipoprotein lipase (LPL) and hepatic endothelial lipase (HL). Whatever their molecular weight, the triacylglycerols of the emulsions were hydrolyzed by LPL and HL. However, the reaction was faster with medium-chain triglycerides (MCT) than with long-chain triglycerides (LCT). To be active, LPL required the presence of serum (apolipoprotein CII); for maximum activity less serum was required for MCT than for LCT. In the case of HL, serum inhibited the effect on LCT but not on MCT. However, hydrolysis of emulsified triacylglycerols by LPL and HL required the presence of albumin as a transporter of the fatty acids released. Less albumin was needed for maximum activity with MCT than with LCT. In vivo, although MCT emulsions were eliminated more rapidly than LCT emulsions, the former resulted in a greater increase in plasma concentrations of triacylglycerols and free glycerol than did the latter. This is explained by the fact that MCT provides about 1.8 times more triacylglycerol molecules than the LCT. In vitro, LPL and HL hydrolyzed structured lipids (randomly esterified triacylglycerols of medium- and long-chain fatty acids) slightly less rapidly than they did control lipids, but there was no comparable difference in the blood lipid parameters examined in vivo. Because the MCT emulsions are cleared rapidly, their fatty acids are rapidly made available to the various tissues where they are oxidized.
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PMID:Activities of lipoprotein lipase and hepatic lipase on long- and medium-chain triglyceride emulsions used in parenteral nutrition. 272 90

Isolated, small very low density lipoproteins (VLDL) from males with plasma concentrations of VLDL triglycerides ranging between 0.92 and 8.65 mmol l-1 were incubated with lipoprotein lipase. There were no differences in the size of the VLDL particles isolated from normo-respectively hypertriglyceridaemic plasmas. After incubation, 4.5 +/- 3.5% (mean +/- SD) of the initial glyceride-glycerol remained in the incubate. This amount did not vary with the plasma VLDL concentration. The incubation mixture was separated into three density fractions: VLDL, low density lipoprotein (LDL) and a high density lipoprotein (HDL) respectively. The lipid contents of these were determined. The distribution of cholesterol and phospholipids after lipolysis was highly dependent on the plasma VLDL level. The amount of cholesterol and phospholipids recovered in the LDL density region increased with the rising plasma VLDL level, the correlation coefficients for this relationship were 0.80 and 0.66, respectively. The results thus indicate that small, similar size VLDL from normo-respectively hypertriglyceridaemic plasmas have different properties.
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PMID:In-vitro lipolysis of small very low density lipoproteins from human plasma. Dependence of characteristics of end products on the serum triglyceride concentration. 273 74

The low-density-lipoprotein (LDL) receptor is a cell-surface protein that plays an important part in the metabolism of cholesterol by mediating the uptake of LDL from plasma into cells. Although LDL particles bind to the LDL receptor through their apolipoprotein B (apo B) and apolipoprotein E (apo E) moieties, other apo E-containing particles, like chylomicron remnants, are not dependent on the LDL receptor for uptake into cells. Chylomicrons formed in the intestinal mucosa during the absorption of the products of digestion, are processed by the peripheral circulation by lipoprotein lipase, which catalyses the breakdown of triglycerides in chylomicrons to free fatty acids and glycerol. The resulting chylomicron remnants, which are cholesterol-rich lipoproteins, are subsequently taken up in the liver. A second distinct protein that binds to apo E-containing lipoproteins, but not to LDL, has been proposed to be the receptor mediating the clearance of chylomicron remnants from the plasma. This protein has a relative molecular mass (Mr) of 56,000 (56K). More recent studies have failed, however, to establish whether this protein is a cell-surface receptor. Here we describe crosslinking experiments in which apo E liposomes were found to bind specifically to the cell surface of hepG2 cells and to human liver membranes. The size and immunological cross-reactivity of the protein to which the liposomes bound was indistinguishable from that of the recently cloned and sequenced LDL-receptor-related protein, LRP. We therefore conclude that the LRP might function as an apo E receptor.
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PMID:The LDL-receptor-related protein, LRP, is an apolipoprotein E-binding protein. 277 54


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