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)

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

Improvement in the method of heart cell cultures is described and justified in relation to environmental factors. The validity of such cardiac cell culture for cardiac research is discussed in light of particular cellular activities: differentiation of lipoprotein lipase, myoglobin biosynthesis, glucose and fatty acid metabolism pleiotypic responses (rotein, RNA, and DNA biosyntheses, substrates transports) to serum stimulation, and the architectonic growth of muscle and nonmuscle cells.
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PMID:Effect of environmental factors and tissue culture methodology in producing and studying cultured cardiac cells. 103 17

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

1. The oral administration of propan-2-ol [isopropanol; 100 mmol (6 g)/kg body weight] or ethanol [130 mmol (6 g)/kg body weight] to starved rats produced no change in plasma post-heparin lipase activity (PHLA) compared with that observed in 154 mmol/1 sodium chloride (saline)-treated rats. 2. An increase of adipose tissue lipoprotein lipase (LLA) and a decrease of heart LLA occurred in isopropanol-treated animals, whereas no significant changes were found in these activities after ethanol administration. 3. Since administration of isopropanol produces hyperglycaemia, observations were also made in rats receiving glucose infusion rather than saline. In these animals a rise in PHLA and adipose tissue LLA, and a fall in heart LLA, occurred. 4. It is suggested that the changes in tissue LLA produced by isopropanol are mediated by the rise in blood glucose.
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PMID:Modifications of plasma post-heparin lipolytic activity and tissue lipoprotein lipase activity induced in the rat by acute administration of ethanol or propan-2-ol. 111 33

Release of lipoprotein lipase from rat fat cells incubated at 20 degrees in medium with albumin, but without glucose proceeded at a constant rate for 30 min. The initial rate of release was increased when serum was present in the medium. Maximal stimulation (100-300%) was produced with 3.8% serum. The maximal increment in release caused by serum was always greater than that produced by heparin and when both were added release was greater than it was with either one alone. The active component(s) of serum, nondialyzable and stable for 30 min at 56 degrees C, was present in sera from humans and rats in the fed or fasted state. Glucose plus insulin (but neither alone) enhanced the rate of lipase release in the presence of serum but not in its absence. The half-life of the lipase in basal medium of 20 degrees C was 90 min. Heparin decreased this to about 50 min and serum markedly prolonged it whether or not heparin was present. Lipoprotein lipase activity in cells and fractions thereof was assayed in extracts of acetone powders. After centrifugation of fat cell homogenates at 600 times g for 15 min, only 50-60% of the activity was recovered in the supernatant. After centrifugation at 100 000 times g for 60 min, the supernatant contained about 10% of the total activity and the sediment 40%. In some experiments, most of the rest was recovered in the floating fat fraction. Total lipoprotein lipase activity of cells plus medium increased steadily during incubation of fat cells for 1h at 30 degrees C. The major increment occurred in the cells and activity in the medium was always less than 15% of the total. Our observations are consistent with the view that activation may be an important determinant of fat cell lipoprotein lipase activity as well as an integral part of the release process.
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PMID:Release of lipoprotein lipase from fat cells in vitro. 112 15

In 13 obese children plasma triglyceride concentrations were found to be significantly elevated, while plasma cholesterol concentrations were normal. In the hypertriglyceridemic obese children, the plasma fractional triglyceride removal, measured by the intravenous fat tolerance test, was significantly reduced. These abnormalities reverted to normal in 8 patients retested after weight loss. Plasma postheparin lipoprotein lipase activity was found to be increased and significantly related to the degree of obesity. As to carbohydrate metabolism, a decreased glucose tolerance and hyperinsulinemia were found. Hyperinsulinemia reverted to normal during dietary restriction, glucose intolerance did not.
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PMID:Plasma triglyceride clearing in obese children. 114 45

To test whether abnormalities in multiphasic release of lipoprotein lipase are associated with hypertriglyceridemia in diabetes mellitus, postheparin lipolytic activity (PHLA) was measured during a high-dose, constant heparin infusion in 20 diabetic subjects with hypertriglyceridemia, 25 nondiabetic hypertriglyceridemic subjects and 7 normal subjects. The standard low heparin dose PHLA and the PHLa during the early phase of the heparin infusion were the same in all groups. In constrast, the PHLA during the late phase of the heparin infusion was lower in the 12 untreated diabetic subjects than in the 25 nondiabetic hypertriglyceridemic and the 7 normal subjects (p less than 0.001). An abnormality in late phase PHLA in the untreated diabetic subjects was more apparent when it was compared to the level of PHLA attained during the early phase of the heparin infusion (Equilibrium PHLA/60 min PHLA). The relative PHLA in the late phase of the infusion was lower in the untreated diabetic subjects (0.671 +/- 0.147) than in the nondiabetic hypertriglyceridemic subjects (0.847 +/- 0.019, p less than 0.001), or in the chronically treated diabetic subjects (0.823 +/- 0.108, p less than 0.05). Among the untreated diabetic subjects, increasing fasting glucose levels were associated with both decreasing absolute PHLA levels at the late phase of the infusion (r = 0.61, p less than 0.02) and greater decreases in relative PHLA during the infusion (r = -0.80, p less than 0.001). Treatment of the diabetes with long-term oral sulfonylurea or insulin therapy corrected the abnormality in the late phase PHLA with an associated decrease in plasma triglyceride levels (p less than 0.001). In five subjects with a deficient PHLA response to a standard, low dose of heparin, the PHLA response was low throughout the heparin infusion. With treatment, the PHLA response to the low heparin dose corrected rapidly toward normal in those two diabetic subjects with PHLa deficiency, and the early PHLA response during the heparin infusion increased. However, the late phase abnormality in all untreated diabetic subjects did not correct to normal until after several months of antihyperglycemic therapy. In the untreated diabetic subjects the degree of elevation of the plasma triglyceride level appeared to result from the interaction of the abnormality in PHLA with the presence or absence of an inherited familial lipid disorder.
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PMID:Reversible abnormalities in postheparin lipolytic activity during the late phase of release in diabetes mellitus (postheparin lipolytic activity in diabetes). 116 28

Glucose or corn oil was given perorally to fasting, young healthy volunteers, and the time course of acute effects on lipoprotein lipase activity (LLA) in adipose tissue, plasma glycerol, triglyceride, insulin, and blood glucose levels was followed. After glucose intake, adipose tissue LLA increased rapidly, reaching a maximum of 80 per cent above initial level after 2 h. Plasma glycerol, reflecting the rate of lipolysis of depot lipids, decreased rapidly, temporally well correlated to the LLA changes. After corn oil intake no significant effect on any of the parameters studied was observed except for an increase in the plasma triglyceride level caused by the influx of dietary lipid.
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PMID:Rapid effect on lipoprotein lipase activity in adipose tissue of humans after carbohydrate and lipid intake. 118 92

In order to define specific metabolic abnormalities of adipose tissue metabolism in endogenous hypertriglyceridemia (EH) patients with this condition were compared with normolipidemic controls matched for body fat and fat cell size. In vitro the enlarged fat cells of EH were found to have an increased basal and noradrenaline-stimulated lipolysis in comparison with cells of the same size from normolipidemic controls. The insulin inhibition of noradrenaline-stimulated lipolysis was blunted. Lipoprotein lipase activity in these cells was clearly depressed. Basal triglyceride synthesis from labeled glucose was low in relation to plasma insulin. The reduction of insulin tolerance in vivo suggested that the depression of plasma glycerol and free fatty acid concentration was small in EH, suggesting that the more detailed findings in vitro were of relevance for in vivo conditions. It was suggested that the hyperinsulinemia and decreased glucose tolerance of EH may well be responsible for some of the aberrations of adipocyte metabolism in EH. The decreased responsiveness of lipolysis to insulin and the low lipoprotein lipase activity are, however, findings not typical for enlarged fat cells exposed chronically to insulin and might be characteristic for the fat cells of EH. It seems of importance to further define the factor(s) responsible for these metabolic aberrations, because the abnormalities of the acipocyte metabolism in EH may well offer a possible explanation to the pathogenesis of that condition.
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PMID:Adipocyte metabolism in endogenous hypertriglyceridemia. 119 32

Lean mice were made obese by feeding, ad libitum, a high-lard diet. They showed an increased fat cell size and number which were maintained when this diet was replaced by the control high-carbohydrate diet for 10 weeks. Obese fed mice showed normal glucose and insulin serum levels, but insulinaemia was elevated after an overnight fast. The insulinaemic response after intraperitoneal injection of glucose was insignificant. Thus hyperinsulinism is not a prerequisite for the development of obesity. High-fat diet influenced, in vitro, glucose metabolism of adipose tissue, liver and muscle: basal lipogenesis was markedly reduced in adipose tissue and liver, and glucose oxidation was decreased in muscle. Insulin sensitivity was reduced by increased fat cell size. De novo formation of fatty acids in liver and adipose tissue did not contribute to the development of obesity. The increased lipoprotein lipase activity of the large fat cells suggested that obesity resulted from a direct storage of dietary fatty acids esterified by glycerol formed from circulating glucose.
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PMID:Metabolism of the mouse made obese by a high-fat diet. 123 69


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