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)

Analysis of plasma lipids of 30- and 185-day-old BIO 82.62 myopathic hamsters and age-matched normal controls revealed a decrease in only the concentration of cholesteryl esters of 185-day-old diseased animals. Measurement of lipoprotein lipase (LPL) activity in heart, muscle, and adipose tissue showed no difference between the activity of the enzyme in the heart and muscle of the cardiomyopathic hamsters and that of the age-matched controls. In adipose tissue, however, LPL activity was depressed in the diseased animals in both age groups. No difference was found in the activity of hormone sensitive lipase. Incorporation of sn[U-14C] glycerol-3-phosphate into total lipids was found to be depressed in homogenates of heart, muscle, and adipose tissue but unchanged in liver homogenates of diseased animals. It was concluded that the decrease in the capacity to synthesize glycerides, rather than limiting substrate concentrations, could be the cause of the decrease in the lipid content in some tissues of the cardiomyopathic hamster.
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PMID:Glyceride metabolism in the myopathic hamster. 89 3

Two trioleoyl glycerol hydrolases, one of lysosomal origin as determined by a high correlation with the lysosomal marker enzyme, N-acetyl-beta-glucosaminidase, and one having the characteristics of lipoprotein lipase, were measured at varying stages of lesion development in the aortas of cholesterol-fed rabbits. Both lipases were greatly enhanced in atheromatous aortas and were linearly related to lesion severity as measured by total aortic cholesterol. Lipoprotein lipase activities of myocardium and of plasma of cholesterol-fed rabbits were also significantly increased relative to controls. The data suggest that lipoprotein lipase might be a factor regulating cholesterol deposition in the aorta.
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PMID:Effect of cholesterol feeding on arterial lipolytic activity in the rabbit. 90 18

The stereochemical course of in vivo hydrolysis of triacylglycerols by lipoprotein lipase was investigated by determining the structure of diacylglycerol intermediates in postheparin plasma of rats which had been fed [3H]glycerol-labeled Intralipid 2 h before an injection of heparin or had been given an injection of a mixture of [3H]glycerol-Intralipid and heparin. During the clearance of both the natural chylomicrons and the artificial emulsion, sn-2,3-diacylglycerols (60-80%) were found to be the dominant enantiomers. Similar results were obtained when the contribution of the hepatic lipase was altered, either by tying off the mesentery artery and portal vein before injection of heparin, or by injection of heparin directly into the portal vein. These findings are consistent with a preferential release of the acyl group from the sn-1 position of the triacylglycerol molecule as demonstrated previously in vitro. A preferential orientation of the substrate in the enzyme-substrate complex or at the oil-water interface is discussed as a possible basis for these effects.
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PMID:Preferential in vivo accumulation of sn-2,3-diacylglycerols in postheparin plasma of rats. 91 99

The nature of the lipolytic activity released from chicken livers perfused with Krebs-Ringer buffer (pH 7.0) containing heparin (50 or 10 U/ml), fraction V albumin (3%), and glycerol (20%) was investigated. The nonrecirculating perfusates contained both previously described NaCl-resistant "liver lipase" as well as an apoLp-Gluactivated lipoprotein lipase (LPL). Crude perfusate lipolytic activity was separated on heparin-Sepharose columns into two enzymatic peaks which were eluted at mean NaCl molarities of 0.75 M (liver lipase) and 1.2 M (LPL). The liver LPL activity was stimulated 7-fold by human apoLp-Glu (half maximal activity at 1.5 microgram/ml) and inhibited by apoLp-Ala, apoLp-Ser, apoLp-GlnI, and apoLP-GlnII. Liver LPL was fully inhibited by anti-adipose LPL immunoglobulins. The "liver lipase" was not affected by apoLp-Glu (3-34 microgram/ml) or anti-adipose LPL immunoglobulins. The data demonstrate the presence in liver perfusates of a LPL with properties similar to adipose tissue lipoprotein lipase.
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PMID:Identification of an adipose tissue-like lipoprotein lipase in perfusates of chicken liver. 92 21

The role of lipoprotein lipase in the uptake of chylomicron triacylglycerol and cholesterol from blood was studied in perfused inguinal-abdominal mammary tissue of rats lactating 10-15 days. Lipoprotein lipase activity in the tissue was reduced, from 0.47 to 0.10 units/g, by removing the anterior pituitary gland from lactating rats 2 days before the experiment. Perfused mammary tissue of normal lactating rats took up 12% of the chylomicron triacylglycerol infused, whereas the tissue of hypophysectomized lactating rats took up less than 1%. About two-thirds of the triacylglycerol taken up was retained as glyceride, and the rest was hydrolyzed and released to the perfusing fluid as fatty acids and glycerol. Autoradiographic studies of perfused tissues of normal lactating rats showed that both the acyl and glycerol moieties derived from chylomicron triacylglycerol were incorporated into milk lipid droplets. Perfused mammary tissue of normal lactating rats also took up 15% of the chylomicron cholesterol infused, whereas the tissue of hypophysectomized lactating rats took up less than 1%. The findings demonstrate that chylomicron cholesterol is taken up with triacylglycerol by lactating mammary tissue, and that uptake of both lipids is markedly suppressed when lipoprotein lipase activity is low, as in tissue of hypophysectomized rats. It is proposed that uptake of triacylglycerol from chylomicrons by mammary tissue requires the action of lipoprotein lipase, while uptake of cholesterol is dependent on reduction of the triacylglycerol core, resulting from action of the enzyme on the core and uptake of lipolytic products by the tissue.
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PMID:Lipoprotein lipase and uptake of chylomicron triacylglycerol and cholesterol by perfused rat mammary tissue. 94 89

The effects of lipoprotein lipase, phospholipase A2 and phospholipase C on chylomicron phosphatidylcholine and triacylglycerol were studied with rat lymph chylomicrons containing phosphatidylcholine labeled with [14C]oleic acid. Lipoprotein lipase purified from bovine milk readily hydrolyzed chylomicron phosphatidylcholine to lysophosphatidylcholine and fatty acid, and triacylglycerol to monoacylglycerol, fatty acid and glycerol. The rates of hydrolysis of phosphatidylcholine and triacylglycerol increased with enzyme concentration, and both decreased when fatty-acid binding sites on albumin in the incubation medium were limited. The proportion and amount of phosphatidylcholine hydrolyzed was always less than that of triacylglycerol. Analyses of hydrolytic products showed that lipoprotein lipase cleaved the 1-acyl ester bond of phosphatidylcholine. The findings indicate that lipoprotein lipase can account for some of the phospholipase A1 activity found in postheparin plasma. Phospholipase A2 and phospholipase C hydrolyzed chylomicron phosphatidylcholine, greater than 92% in 10 min, but not triacylglycerol. The resultant phosphatidylcholine-deficient chylomicrons, which could be concentrated by ultra-centrifugation and resuspended in incubation medium, were readily depleted of triacylglycerol when incubated with lipoprotein lipase. The findings indicate that phosphatidylcholine can be removed from the surface film of chylomicrons without disrupting the particles or blocking the action of lipoprotein lipase on the core triacylglycerol.
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PMID:Hydrolysis of chylomicron phosphatidylcholine in vitro by lipoprotein lipase, phospholipase A2 and phospholipase C. 94 90

Destruction of the ventromedial hypothalamic nuclei (VMN) in the weanling rat without injury to the median eminence results in a series of somatic, endocrine, and metabolic changes that are characterized by normal food and water intake but decreased linear growth, normal body weight but increased carcass fat and reduced carcass protein, lean body mass, and water. The endocrine alterations comprise hyperinsulinemia in the face of normoglycemia, hypertriglyceridemia and hypercholesterolemia and reduced growth hormone levels. The metabolic changes include greater oxidation of glucose and incorporation into lipid and reduced palmitate oxidation but increased incorporation into lipid. Weanling rats with VMN lesions are normophagic in absolute terms, relative to body weight and per metabolic unit, but their nocturnal feeding and weight gain cycles are disrupted and their locomotor activity is reduced. The VMN are involved in the long-term control of feeding - as in the mature rat - as shown by intragastric preloading studies and dietary density manipulation, glucose preference tests and intraperitoneal injections with glucose. Hyperinsulinemia and hypertriglyceridemia are present four days after the VMN operation in the presence of subnormal food intake and plasma glucose levels. Manipulations of the fat content of the diet revealed that the hyperlipidemia is of both endogenous and exogenous origin and that lipoprotein lipase is increased; a 48-hour fast reduced the hyperlipidemia to control levels, however. This suggests that weanling VMN rat tissue may have an impaired ability to take up circulating lipid. An increased incorporation of glycerol into lipid may be due to induction of glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per milligram of tissue protein. Glucose oxidation and incorporation into adipose tissue is increased in several tissues in vitro and there is enhanced glucose disappearance from plasma and incorporation into tissue lipids in vivo. These changes develop within a short time after lesion production and persist at least partially up to six months: glucose utilization in liver increases already four hours after the operation whereas it takes 72 hours to commence in adipose tissue. Insulin resistance is not apparent either in vivo or in vitro. The decreased growth hormone levels are not critical to the metabolic changes, nor is the hyperinsulinemia totally necessary. The metabolic changes also appear on several different types of diet and persist with fasting. The latter does not reduce insulin sensitivity of VMN rat tissues, wheras it does so in normal rats. Mature rats developed the same metabolic changes even in the absence of hyperphagia. The metabolic alterations can be blocked by pharmacologic doses of glucocorticoids, but are enhanced by the administration of estrogen...
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PMID:Origin of endocrine-metabolic changes in the weanling rat ventromedial syndrome. 95 Jun 80

Fatty acid incorporation into adipose tissue (FIAT), the metabolic process assimilating plasma triglyceride fatty acids liberated by lipoprotein lipase, was recently found to be lower in hyper- than in normotriglyceridaemia. In the present report, the relation of FIAT to glucose tolerance and adipose tissue morphology and fatty acid composition has been studied in a popoulation of men with normo- and hypertriglyceridaemia, using needle biopsy specimens. In addition, the associations between plasma triglyceride concentration and these factors as well as FIAT were examined by statistical methods. FIAT and GLIAT (glucose incorporation into adipose tissue) activities per cell were positively correlated with fat cell diameter but not with fat cell number. FIAT activities per cell and per unit surface area were lower in hyper- than in normo-triglyceridaemic subjects. The k-value of the i.v.glucose tolerance test and glycerol release from adipose tissue did not correlate with FIAT or GLIAT activities. The proportion of stearic acid in adipose tissue was negatively correlated with the serum triglyceride level and with fat cell diameter, but positively correlated with FIAT. Linolenic acid in adipose tissue correlated positively with the k-value. The negative correlation between serum triglycerides and FIAT remained when the other variables which were significantly correlated with FIAT or the serum triglycerides were entered in partial correlat-on analysis. These results suggest that although low FIAT activity is related in part to other characteristics, it occurs in hypertriglyceridaemia independent of glucose tolerance or various characteristics in fat. With serum triglyceride concentration as dependent variable, stepwise regression analysis was performed, entering all other variables as independent ones. The highest multiple --value was 0.76 (p less than 0.001) and it was obtained with three adipose tissue parameters: FIAT (or GLIAT), content of linolenic acid and of stearic acid. The other parameters did not give rise to any further improvement in the prediction of the serum triglyceride concentration which is better than 50% (R2 = 0.57).
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PMID:Serum triglycerides and fatty acid incorporation into human adipose tissue (TIAT). Their relations with adipose tissue characteristics and glucose tolerance. 98 13

Fat-mobilizing lipolysis was studied in rat and human adipose tissue during incubation in vitro by following the release of glycerol into the incubation medium. Gemfibrozil as well as clofibrate consistently and readily inhibited basal as well as noradrenaline-stimulated fat-mobilizing lipolysis in rat fat. With human adipose tissue no effect was observed with gemfibrozil and clofibrate on basal lipolysis. This may be due to the comparatively low rate of the nonstimulated fat-mobilizing lipolysis in human tissue incubated in vitro. When lipolysis was stimulated with noradrenaline as well as isoprenaline, however, both gemfibrozil and clofibrate significantly reduced the fat-mobilizing lipolysis. This inhibition of lipolysis was however not observed in all studies. When lipolysis had been stimulated with theophylline, no inhibition of lipolysis was obtained with either compound. The possibility that reduced fat-mobilizing lipolysis in adipose tissue may cause a lowering of plasma triglycerides by reducing the flow of FFA to the liver is discussed in some detail. It is also suggested that inhibition of lipolysis may be accompanied by increased activity of lipoprotein lipase as well as an increase in the FIAT process. However, the pharmacological implication of the above-mentioned findings, particularly for gemfibrozil, must await further studies, as fairly large doses, around 1 mg/ml of incubation medium, were needed to obtain inhibition of fat-mobilizing lipolysis.
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PMID:Effect of gemfibrozil in vitro on fat-mobilizing lipolysis in human adipose tissue. 101 47

Intravenous injection of heparin increases lipoprotein lipase activity of circulating serum presumably by removing the enzyme from its location on the capillary endothelium. The incorporation of carbon-14 uniformly labeled glucose and carbon-14 1-labeled palmitic acid into fractionated milk fat triglycerides was studied in both normal and heparin treated lactating goats. The objective was to remove lipoprotein lipase from the mammary gland capillaries and to contrast normal milk fat synthesis with a situation presumed to cause the gland to be solely dependent on the phosphatidic acid pathway. The studies with labeled glucose indicated that under normal conditions there are two sources of milk glyceride glycerol; while following heparin injections, there is a single glycerol pool providing most of the glyceride glycerol. The investigations with labeled palmitic acid indicated that under normal conditions there are two sources of palmitic acid coming from the blood which enter nonequilibrating cellular pools. Palmitic acid from both pools is available for triglyceride synthesis. Following heparin injections there appears to be a common intracellular pool of pre-formed palmitic acid derived from the blood. The data indicate that lipoprotein lipase operating on blood triglycerides yields a 2-mono-glyceride which subsequently enters the gland and is utilized for milk fat synthesis.
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PMID:Structure and synthesis of milk fat XI. Effects of heparin on paths of incorporation of glucose and palmitic acid into milk fat. 111 40


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