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)

Chylomicrons isolated from rat lymph were complexed with lipoprotein lipase of post-heparin plasma (chylomicrons-LPL) in order to study the effects of lipolysis on the structure of chylomicrons. Triglyceride in the chylomicron core was readily hydrolyzed to free fatty acids (FFA) and glycerol when chylomicrons-LPL were incubated at pH 8.3 in medium containing albumin. Although most of the FFA were immediately released to the medium, some were retained within chylomicrons when FFA-binding sites on albumin were not available. These observations suggest that albumin may have a specific role in the transfer of FFA across the chylomicron surface film. Chylomicrons-LPL assumed many different shapes as they were depleted of triglyceride by the lipolytic action of the enzyme, and total removal of core triglyceride resulted in empty sacks of surface film. The surface film was visualized in sections of OsO(4)-fixed chylomicrons-LPL as a thin electron-opaque line, 25-30 A wide, in areas where the underlying electron-opaque core had been replaced by zones of decreased electron opacity, and in folds of surface film extending outward from chylomicrons partially depleted of core lipid. The findings demonstrate that chylomicrons consist of a core of liquid triglyceride enveloped by a pliable and durable monolayer surface film, and that lipoprotein lipase reduces the triglyceride core without disrupting the surface film.
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PMID:Effects of lipoprotein lipase on the structure of chylomicrons. 474 23

When NH(4)OH-NH(4)Cl extracts of adipose acetone powder were applied to agarose gel chromatography columns, two peaks of lipoprotein lipase were eluted. The first activity peak (LPL(a)) was eluted with an elution volume of a protein of molecular weight approximately five times that of the second (LPL(b)). Addition of heparin to the eluted fractions markedly stimulated activity of LPL(a), but suppressed that of LPL(b). Both lipases had the characteristics that distinguish lipoprotein lipase from other tissue lipases: a requirement for serum for substrate activation, inhibition by 1 m NaCl, and an alkaline pH optimum (pH 8.0). It is concluded that these fractions represent two species of lipoprotein lipase.
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PMID:Separation of molecular species of lipoprotein lipase from adipose tissue. 505

The role of LPL in reducing the serum triacylglycerol concentration was investigated in rats fed a high sucrose diet containing 0.25% (w/w) ethyl-CPIB. Compared with sucrose-fed controls, drug treatment resulted in a fall in adipose tissue LPL activity and a rise in enzyme activity in thigh and heart muscle. Serum post-heparin lipoprotein lipase activity after a high dose of heparin was lower in ethyl-CPIB-treated rats than controls, but after a low dose of heparin the values were similar. The amount of LPL activator was decreased by the drug. Thus, the low serum triacylglycerol concentration observed in the ethyl-CPIB-treated rats cannot be explained by changes in functional LPL activity. The plasma triacylglycerol-lowering effect of the drug could be explained by the observed decrease in triacylglyerol output by the liver.
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PMID:Effects of ethyl-CPIB (clofibrate) on tissue lipoprotein lipase and plasma post-heparin lipolytic activity in rats. 637 Feb 67

To explore the mechanism whereby stanozolol, a 17 alpha-methyl androgenic anabolic steroid, depresses high density lipoproteins (HDL), 6 subjects, aged 46-71 yr (4 postmenopausal women and 2 men), underwent paired studies of 125I-HDL turnover (including HDL2 and HDL3 and Apo A-I and A-II) and postheparin plasma (PHP) lipolytic activity (hepatic triglyceride lipase, HTGL, and lipoprotein lipase LPL) before and during treatment with stanozolol, 6 mg/day. While total cholesterol and triglyceride levels did not change during stanozolol, HDL-cholesterol decreased from 59 +/- 18 mg/dl (x +/- SD) to 29 +/- 7 mg/dl (p less than 0.01) and low density lipoprotein (LDL)-cholesterol increased from 160 +/- 36 mg/dl to 181 +/- 42 mg/dl (p less than 0.02). PHP-HTGL increased from 111 +/- 47 nmole/min/ml to 369 +/- 202 nmole/min/ml (p less than 0.04), while PHP-LPL did not change. At baseline the residence time of HDL2 (4.00 +/- 1.04 day) was shorter than that of HDL3 (6.79 +/- 1.00 day) (p less than 0.001). Residence times of both declined on stanozolol, to 3.25 +/- 0.83 day and 4.00 +/- 0.29 day, respectively (0.1 less than p less than 0.2); however, only the reduction in residence time of HDL3 was statistically significant (p less than 0.001). At baseline the residence time of apo A-I (4.93 +/- 1.32 day) was shorter than that of A-II (6.85 +/- 1.98 day) (p less than 0.025); on stanozolol these declined to 3.19 +/- 0.41 (p less than 0.02) and 5.10 +/- 1.13 (p = 0.07), respectively, still significantly different from each other (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on the metabolic mechanism of reduced high density lipoproteins during anabolic steroid therapy. 641 14

In two separate trials male and female Wistar rats, 12 weeks of age, were either killed as a preliminary control group, ad lib.-fed or undernourished for 4 weeks until one-third of their 12-week body-weight was lost. Food intakes, urinary and faecal collections and measurements of standard metabolic rate were made at one-weekly intervals on both the ad lib.-fed and undernourished animals of both sexes. The bodies of the preliminary controls, the ad lib.-fed and the undernourished animals of both sexes were analysed for protein and fat, and the weights of four fat depots, two muscles and the major organs of all groups were determined. Measurements of lipid synthesis rate (LSR) and lipoprotein lipase (EC 3.1.1.34) (LPL) activity in the four fat depots and measurements of whole-body protein synthesis rates were carried out on animals of both sexes in each group. Although both sexes lost the same proportion of body-weight the females required more food on a body-weight basis than the males during the undernutrition period. The females absorbed significantly more energy on a body-weight basis during undernutrition and so were less efficient than the males at withstanding nutritional stress. There were no significant differences between males and females, on a body-weight basis, in the excretion of nitrogenous waste products (urinary nitrogen, creatinine, hydroxyproline or NT-methylhistidine) suggesting that there were no differences between the sexes in protein sparing during undernutrition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of male and female rats to undernutrition. 1. Changes in energy utilization, body composition and tissue turnover during undernutrition. 647 63

Serum lipoproteins were measured during a single infusion of intralipid and during parenteral nutrition with intralipid and glucose. Postheparin plasma lipolytic enzymes and plasma LCAT activity were assayed before and after the parenteral nutrition. Both single and repeated infusions of intralipid were followed by a significant rise of HDL2 concentration (p less than 0.01), whereas the HDL3 decreased. The composition of HDL subclasses altered. The HDL2 triglyceride and phospholipids increased, while the HDL3 esterified cholesterol and protein decreased. In vitro incubation of serum with intralipid alone caused no changes in the zonal profile of HDL subclasses, but hydrolysis of intralipid by lipoprotein lipase was followed by conversion of HDL3 into lighter particles floating in the density range of HDL2. The present results provide additional evidence for a precursor-product relationship between the HDL2 and HDL3. During 4 days of parenteral nutrition with intralipid, the basal (morning) values of serum total and VLDL triglyceride did not change. The LDL phospholipids increased progressively (from 67 to 98 mg/dl, p less than 0.05). The total HDL cholesterol decreased and this change was due to the fall of HDL3 cholesterol esters (from 19 to 12 mg/dl, p less than 0.05). Also the basal values of apo A-I and A-II in HDL3 decreased. The basal level of the HDL2 remained constant. Postheparin plasma LPL activity increased by 52% (p less than 0.01) but hepatic lipase activity fell by 49% (p less than 0.05). These changes may account for the maintenance of plasma HDL2, whereas the progressive fall of the basal HDL3 is probably due to the lack of intestinal apoprotein synthesis during absent intestinal absorption.
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PMID:Changes of high density lipoprotein subfraction concentration and composition by intralipid in vivo and by lipolysis of intralipid in vitro. 665 16

Experiments on rabbits have shown hyperlipidemia to develop within the first 48 h after a single intravenous injection of bovine serum albumin (BSA, fraction V). The mean concentration of blood plasma triglycerides (TG) was considerably higher than normal (by 262% after 24 and by 625% after 48 h). The cholesterol content was also elevated (by 80 and 270%, respectively). Following 7 and 14 days the lipid concentration returned to normal. The plasma post-heparin lipoprotein lipase activity (PHP-LPL) was lower 24 h and 7 days after BSA injection and the hypotriglyceridemic effect of heparin was less pronounced. The data obtained support the hypothesis that hyperlipidemia provoked by a single intravenous injection of BSA to rabbits results from low PHP-LPL activity and possible changes in TG-rich lipoprotein substrate affinity for the enzyme.
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PMID:[Role of lipolytic enzymes in the development of hyperlipidemia induced by administration of heterologous albumin in rabbits]. 669 22

The relationship between obesity and alterations in adipose tissue metabolism and lipid transport was studied in fourteen obese subjects before and after a weight reduction of 4-22 kg. Blood glucose and plasma insulin patterns after peroral glucose intake improved significantly, and plasma glucagon levels decreased markedly after treatment. Plasma triglyceride and total cholesterol levels were not altered, but there was a 20% (P less than 0.05) increase in HDL concentrations. Plasma free fatty acid and glycerol concentrations decreased, in parallel to a decrease in lipolysis rate in vitro. Lipoprotein lipase and hepatic lipase activities in postheparin plasma, as well as the intravenous fat tolerance test, were normal and did not change significantly after weight loss. Lipoprotein lipase activity in adipose tissue, expressed per cell, was elevated and did not change after weight reduction. Also, the enzyme activity did not increase after glucose intake before or after treatment. The lack of effect on lipoprotein lipase activity and regulation in combination with significant improvements of other aspects of lipid and glucose transport is consistent with the view that alterations in LPL activity and regulation may represent an early and possibly primary defect in the development of obesity.
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PMID:Effects of weight reduction on plasma lipoproteins and adipose tissue metabolism in obese subjects. 680 Aug 25

Immunochemical methods for selective measurement of lipoprotein lipase and hepatic lipase activities in rat postheparin plasma are described and validated. Lipoprotein lipase was measured using a substrate containing 10% serum and 0.1 M NaCl after inactivation of hepatic lipase with a specific antiserum. Hepatic lipase was measured at 1.0 M NaCl with a serum-free substrate. The heparin dose-response curve indicated maximum relase of both activities at a heparin dose of 500 IU/kg. The lipase activities in rat postheparin plasma were 3 to 4-fold higher than those in human postheparin plasma. The LPL activity in female rats was significantly higher than in males whereas there was no sex difference for hapatic lipase.
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PMID:Immunochemical assay of rat postheparin plasma triacylglycerol lipases. 699 Sep 38

These studies were initiated to see if factors other than reduced lipoprotein lipase activity might contribute to the defect in plasma removal of very low density lipoprotein (VLDL) that is observed in insulin-deficient rats. VLDL-triglyceride (TG) was labeled in vivo with 3H-glycerol in control and diabetic rats, and aliquots of plasma containing 3H-VLDL were injected into normal recipient rats. The half-time (t 1/2) of removal was almost twice as long when plasma from diabetic rats was injected, and this was true when the diabetic rats were fed either sucrose or regular chow. A comparable increase in t 1/2 was observed when 3H-VLDL isolated from normal rats was recombined with VLDL-free plasma from control and diabetic rats and injected into normal recipients. As before, the changes observed were not dependent upon antecedent diet. However, no significant difference in t 1/2 was observed when 3H-VLDL was isolated from control and diabetic rats and injected into normal recipients. Thus, there appears to be a factor present in VLDL-free plasma obtained from diabetic rats that interferes with removal of VLDL from the vascular compartment. Whether this factor is found in diabetic plasma in vivo, or is transferred from diabetic VLDL to diabetic plasma in the isolation procedure, remains to be clarified. In either event, there appears to be a factor, other than reduced LPL activity, that may play a role in the defect of VLDL-TG removal seen in insulin deficiency.
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PMID:Evidence for a new cause of defective plasma removal of very low density lipoproteins in insulin-deficient rats. 701 12


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