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)

Diurnal plasma lipids and lipoproteins were studied in twelve healthy young males on corn oil and palm oil diets, respectively. The major triglyceridy. Lecithin-cholesterol acyl transferase, lipoprotein lipase and hepatic triglyceride lipase were also measured. diurnal changes of triglycerides and cholesterol were confined to lipoproteins of d less than 1.006 kg/l. There was a diurnal rise of lecithin-cholesterol acyl transferase activity with corn oil but not with palm oil. Fasting and postprandial postheparin lipoprotein lipase and hepatic triglyceride lipase were similar but there was a significant correlation of postprandial hepatic lipase with postprandial plasma triglycerides on palm oil. Marked diurnal changes of triglyceride fatty acids were observed not only in 'very low density lipoprotein' but also in high-density lipoprotein amounting to approximately one third of total high density lipoprotein triglyceride fatty acids.
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PMID:Acute dietary effects on plasma lipids, lipoproteins and lipolytic enzymes in healthy normal males. 11 24

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.
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PMID:Changes in aortic glycosaminoglycans and lipoprotein lipase activity in rats with age and atheroma. 12 74

This paper shows that the palmitoyl-CoA hydrolase activity of postheparin serum of the rat is mainly derived from the liver. The identity of this activity with the heparin-releasable hepatic triacylglycerol hydrolase activity is established. The consequences of the different substrate specificities of the hepatic and extrahepatic enzymes for the measurement of the overall postheparin serum lipase activity are discussed. Treatment of the rats with either a corticosteroid or with streptozotocin was found to lower the lipolytic activity from the liver and to enhance the extrahepatic activity. Also in human postheparin serum, palmitoyl-CoA hydrolase activity is shown to behave identical with hepatic triacylglycerol hydrolase activity. The possible function of the liver in the serum triacylglycerol metabolism is discussed in connection with the proposed mechanism for the role of extrahepatic lipoprotein lipase in atherogenesis.
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PMID:On hepatic and extrahepatic postheparin serum lipase activities and the influence of experimental hypercortisolism and diabetes on these activities. 12 97

The effect of hormone administration on the activity of lipoprotein lipase in the lung was studied in the rat. The following hormones were administered: dexamethasone, L-thyroxine, estradiol-17beta and progesterone. In addition, lung lipoprotein lipase activity was studied in diabetic and lactating rats. Lipoprotein lipase activity was measured in dried, defatted preparations of rat lung using double labeled ([14C]palmitate, [3H]glycerol) chylomicron triacylglycerol as substrate. Dexamethasone administration caused a rise of 70% in the level of activity of lipoprotein lipase in acetone powders of lung and a 100% increase in the amount of enzyme released during heparin infusion into isolated, perfused lungs. Enzyme activity was higher in lungs of females than of male rats; however; the level of activity was unaffected by estrogen or progesterone administration to either male or ovariectomized rats. Diabetes, hyperthyroidism or lactation did not change lipoprotein lipase activity in the lung. The constant presence of lipoprotein lipase activity in the lung suggests that this organ is able to maintain a steady supply of triacylglycerol-fatty acids under a variety of physiological and pathological conditions. Stimulation of enzyme activity by dexamethasone could lead to increased uptake of triacylglycerol-fatty acids by the lung and may thus be a contributing factor to corticosteroid-induced enhanced surfactant synthesis.
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PMID:Lipoprotein lipase in rat lung. Effect of dexamethasone. 13 65

The activity of hepatic triglyceride lipase in the rat was reduced by fasting. Withdrawal of insulin from insulin-treated streptozotocin-diabetic rats resulted in a decrease in hepatic triglyceride lipase activity. The behavior of the enzyme in both situations was similar to that of adipose tissue lipoprotein lipase. It is concluded that hepatic triglyceride lipase, like adipose tissue lipoprotein lipase, is under hormonal regulation by insulin.
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PMID:The effects of fasting and streptozotocin diabetes on hepatic triglyceride lipase activity in the rat. 13 56

Labeled chylomicrons in thoracic duct lymph were collected after test meals containing 14C cholesterol and 2-3H glyceryl trioleate and were given by intravenous injection to groups of control rats, rats made diabetic by treatment with streptozotocin, and rats made hypothyroid and hypercholesterolemic by a diet containing cholesterol, peanut oil, cholic acid, and thiouracil. In the diabetic rats clearances from the plasma of chylomicron triacylglycerol and cholesteryl ester were impaired. A large variability in triacylglycerol clearance in diabetic rats was ascribed to variability in plasma triacylglycerol concentrations. Adipose tissue lipoprotein lipase activity was not impaired in the female diabetic rats used in this study. In the hypothyroid hypercholesterolemic rats chylomicron cholesteryl ester clearance from the plasma was impaired but chylomicron triacylglycerol was cleared efficiently, and adipose tissue lipoprotein lipase activity was similar to or greater than activity in controls. Ten minutes after intravenous injection most plasma radioactivity was recovered in lipoproteins of density less than 1.006 g/ml in all groups of rats, but relatively more was recovered at this density in both treatment groups. We suggest that chylomicron remnants accumulate in the plasma and contribute to the development of hyperlipemia in both treatment groups, but that the remnants formed in the diabetic rat are less depleted of triacylglycerol than the remnants formed in the hypothyroid hypercholesterolemic rat. It is suggested that factors other than measured lipoprotein lipase activities of adipose tissues may be important in determining the initial extent of hydrolysis of chylomicron triacyglycerol. We propose that the hypercholesterolemic hypothyroid rat is a useful model for the experimental production of the remnants of triacylglycerol-rich primary lipoproteins.
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PMID:Clearance of chylomicron triacylglycerol and cholesteryl ester from the plasma of streptozotocin-induced diabetic and hypercholesterolemic hypothyroid rats. 13 29

Lipase activity extracted from cultured neonatal rat heart cells was characterized and identified as lipoprotein lipase. Enzyme activity was stimulated by human apoC-II and rat serum; serum stimulation was prevented by human apoC-I and by apoC-II. Lipolysis was maximal at pH 8.0 and was inhibited by protamine sulfate, NaCl, and high concentrations of heparin. About 50% of heart cell lipase activity applied to heparin-Sepharose bound to the gel and was eluted with a NaCl gradient. A peak of lipase activity was observed at 0.84 M NaCl. Neonatal rat heart cells in culture are a mixture of muscle and non-muscle cells. To determine the cellular location of the lipoprotein lipase, enzyme activity and muscle cell content of the cultures were determined. Myosin ATPase was used as an index of muscle cell content since ATPase specific activity correlated (r = +0.97) with muscle cell content determined immunofluorescently. When muscle cell content of cultures was decreased or increased by differential plating, lipase specific activity was constant. Moreover, lipase specific activity was constant during culture growth despite a decrease in muscle cell content. It was concluded that lipoprotein lipase activity of cultured heart cells is not associated solely with either muscle or non-muslce cells.
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PMID:Lipoprotein lipase in cultured heart cells: characteristics and cellular location. 13 38

Lipoprotein lipase activity was measured at short time intervals in cardiac and skeletal muscles of normal and streptozotocin-treated diabetic rats fed ad libitum or deprived of food. In normal animals fed ad libitum, lipoprotein lipase activities of heart, diaphragm, soleus, and fast-twitch red fibers of the quadriceps muscle showed rhythmic oscillations that appeared to coincide with the nocturnal feeding habits of the animals. During the day (7 A.M. to 7 P.M.), when food consumption by the rats was greatly reduced, lipoprotein lipase activity in all muscles increased, followed by a decline to basal levels during the night. Similar oscillatory changes in lipoprotein lipase activity were observed in the muscles of diabetic rats fed ad libitum. In normal rats deprived of food, however, the oscillatory changes in muscle lipoprotein lipase activity were not abolished and persisted for at least 48 h. In diabetic rats starved during a 48-h period, the oscillatory changes in muscle lipoprotein lipase activity were markedly altered. In all animals, muscle lipoprotein lipase activities were not correlated to plasma glucagon levels.
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PMID:Oscillatory changes in muscle lipoprotein lipase activity of fed and starved rats. 14 95

The wet weight evolution and specific and total lipoprotein lipase (LPL) activities of the heart were studied in male rats fed with diets containing 4, 12 or 21 p. 100 lipids from 50 g (3 weeks age) to 400 g body weight (13 weeks of age). The animals were compared at 100, 150, 200 and 400 g. The main results show that:--a lipid-rich diet caused some cardiac hypertrophy beginning at 100 g body weight:--specific LPL activity (activity/g of wet tissue) in the 50-400 g interval was higher when the diet contained more lipids;--when the diet contained 4 p. 100 and 12 p. 100 lipids, specific LPL activity decreased from weaning until a plateau was reached at 200 g body weight. On the other hand, when the diet contained 21 p. 100 lipids, specific LPL activity increased to a maximum in the 150-200 g interval; it then declined rapidly so that at 400 g there were no longer significant differences between the specific LPL cardiac activities of the three groups of animals. The activities thus became independant of the dietary lipid level;--total LPL cardiac activity was higher when the diet contained more lipids, at least up to the 400 g stage. When the diet contained 4 and 12 p. 100 lipids, the activity increased linearly in the 100-400 g interval. When the diet contained 21 p. 100 lipids, it increased very rapidly in the 50-200 g interval then decreased in the 200-400 g interval. In the latter interval, the differences between LPL activities of the three groups were less so that at 400 g there was only significant difference between the extreme high and low lipid groups. Thus, as specific activity, total LPL cardiac activity tended to become independent of dietary lipid level when the animals became adult.
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PMID:Post-weaning heart development and dietary lipid level in the male rat: evolution of lipoprotein lipase activity. 15 97

Kinetic studies of the very-low-density lipoprotein triglycerides (VLDL-TG) turnover by endogenous labeling with glycerol-2-3-H were performed in 13 patients in the postabsorptive state, first after 10-14 days on a low-sucrose high-starch diet, then again after 10-14 days of isocaloric high-sucrose low-starch diet (HSD). After HSD, a significant decrease in the fractional turnover rates of VLDL-TG was observed, as well as a modest but significant increase in its pool size, but the net turnover rates remained unchanged. Using Michaelis-Menten formulation, we have further calculated the Vmax and Km's of the removal system for VLDL-TG and found that the Vmax and Km's do not differ significantly between the two dietary periods. These results suggest that the removal mechanism for VLDL-TG has not changed after 10-14 days on the HSD, at least when the patients are studied in the postabsorptive state. Measurements of postheparin lipolytic acitivty under fed condition in 17 patients (including the 13 patients above) have shown a decrease after HSD. However, a defect in the removal of plasma-TG related to decreased activity of tissue-lipoprotein lipase in the fed state has not been conclusively uncovered by the kinetic studies performed in the postabsorptive state, and cannot contribute significantly to the expansion of VLDL-TG pool.
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PMID:Human plasma triglyceride labeling after high sucrose feeding. II. Study on triglyceride kinetics and postheparin lipolytic activity. 16 66


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