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)

This study was conducted to investigate acute effects of smoking on platelet function, endothelial cells and plasma lipids and to follow these parameters after Aspirin ingestion. Twelve fasting smokers each inhaled the smoke of one cigarette. Blood was drawn before and 10 min after smoking. Plasma nicotine, measured by gas chromatography, increased from 13.48 before smoking to 78.41 nM after smoking. Platelet aggregation to thrombin and ADP increased significantly (P less than 0.001). The platelet aggregate ratio decreased from 0.95 to 0.75 (P less than 0.005). Plasma beta-thromboglobulin also increased in post-smoking samples as measured using radioimmunoassay. 'Circulating endothelial cells' increased significantly after smoking (P less than 0.005). Triglycerides decreased (P less than 0.005) in plasma and in the VLDL fraction (P less than 0.05). Both post-smoking plasma free fatty acids and free glycerol increased, respectively, as compared with respective values. Lipase activity ascribable to lipoprotein lipase and hepatic lipase, absent in pre-smoking plasma samples, could be detected in post-smoking plasma without heparin injection. At least 1 week later, the subjects returned to follow an identical protocol except that they had ingested Aspirin (650 mg) 10-14 h before blood sampling. The same parameters were measured before and after smoking the same cigarette. Except for plasma nicotine, all the smoking-induced changes were abolished by ingestion of Aspirin. The results of this study indicate an interrelationship between platelet hyperactivity, endothelial injury and plasma lipids. They also demonstrate an inhibition of the major smoking-induced changes by Aspirin in the presence of high plasma nicotine levels. It is concluded that Aspirin may offset several of the deleterious acute effects of smoking. However, our conclusions cannot be, in any way, extended for long-term effects of both smoking and Aspirin treatment. Based on these data, it is suggested that there may be some links between platelet hyperactivity, endothelium injury and plasma lipids.
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PMID:Acute influence of smoking on platelet behaviour, endothelium and plasma lipids and normalization by aspirin. 146 56

1. Release of endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) from bovine cultured aortic endothelial cells (EC) was measured by bioassay and radioimmunoassay, respectively. 2. Bradykinin (BK, 3-30 pmol), adenosine diphosphate (ADP, 2-6 nmol) or the sodium ionophore monensin (40-100 nmol) injected through a column of EC released EDRF. L-Arginine free base (FB; 10-20 mumol) or D-arginine FB (10-20 mumol) injected through the column of EC released similar amounts of EDRF and also caused an increase in pH of the Krebs solution perfusing the EC from 7.5-8.0 to 8.6-9.5. Sodium carbonate (Na2CO3) an alkaline buffer which caused the same changes in the pH of the Krebs solution also induced the same release of EDRF. The hydrochloride salts of L- or D-arginine did not cause either release of EDRF when injected through the column of EC or increases in the pH of the Krebs solution. 3. Inhibitors of either diacylglycerol lipase (RHC 80267) or kinase (R59022) inhibited the release of EDRF induced by BK or ADP but potentiated the release induced by L-arginine FB, monensin (40-100 nmol) or alkaline buffer (Na2CO3). R59022 and RHC 80267 infused through the EC increased the basal release of EDRF. 4. When calcium chloride was omitted from the Krebs solution the release of EDRF induced by alkaline buffer (Na2CO3; pH 8.6-9.5) or L-arginine FB (10-20 mumol) was selectively inhibited when compared to that induced by BK (3-30 pmol) or ADP (2-6 nmol). This inhibition was reversed when calcium (2.5 mM) was restored. 5. NG-monomethyl-L-arginine (NMMA; 30 microM) inhibited release of EDRF induced by BK (10-30 pmol) or alkaline buffers (Na2CO3 or D-arginine FB; pH 8.6-9.5). This inhibition was partially reversed by L- but not D-arginine FB or HCl (30-100 microM). 6. Prostacyclin was released when BK (10 pmol), ADP (2 nmol) or arachidonic acid (30 nmol) were injected through the column of EC. However, monensin (40 nmol) or alkaline buffers (pH 8.6-9.5) did not release detectable amounts of PGI2 as measured by radioimmunoassay for 6-oxo-prostaglandin F1 alpha. 7. Thus alkalinisation of the external bathing solution can release EDRF from cultured EC by a mechanism which does not involve receptor activation and which depends on the presence of extracellular calcium.
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PMID:Alkaline buffers release EDRF from bovine cultured aortic endothelial cells. 188 92

The guanine nucleotide binding protein (G-protein) dependency of several of the activities of tumor necrosis factor (TNF), including cytotoxicity, inhibition of lipoprotein lipase activity, blockade of 3T3-L1 differentiation, and receptor binding were examined. TNF induced killing of the TNF-sensitive cell line L929S (ED50 = 30 pM), but had little to no effect on the TNF-resistant cell line L929R (ED50 = 5,300 pM). TNF-induced cytotoxicity in L929S was antagonized in a dose-dependent manner by pertussis toxin (sevenfold increase in ED50). However, TNF-induced cytotoxicity in L929R cells was only minimally affected by pretreatment with a high dose (50 ng/ml) of pertussis toxin (1.5-fold increase in ED50). Parallel biochemical investigations revealed that inhibition was accompanied by toxin-induced ADP ribosylation of a Gi alpha-like subunit in L929 and 3T3-L1 cell membranes. Pertussis toxin also significantly reduced TNF-induced inhibition of lipoprotein lipase activity in 3T3-L1 adipocytes and TNF blockade of 3T3-L1 preadipocyte differentiation. However, pertussis toxin pretreatment of L929S, L929R, and 3T3-L1 cell cultures had little to no effect on TNF receptor binding. These data indicate that several TNF-induced biological activities in the L929 and 3T3-L1 cell lines are partially dependent upon a pertussis toxin-sensitive G-protein.
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PMID:Tumor necrosis factor-mediated biological activities involve a G-protein-dependent mechanism. 216 71

Sixteen rabbits were fed a 1% cholesterol diet with an intraperitoneal injection of saline (n = 8) (cholesterol-diet group), or 50 mg glycosaminoglycans-polysulfate (GAG-PS) (n = 8) (GAG-PS group). After 10 weeks all rabbits were sacrificed and studied. Eight rabbits on a standard diet with an intraperitoneal injection of saline (n = 8) (standard-diet group) were processed in the same manner. After 10-weeks of feeding, the plasma total cholesterol of the GAG-PS group was significantly lower than that of lower than that of the control group (P less than 0.02). The VLDL cholesterol of the GAG-PS group was also significantly lower than that of the cholesterol-diet group. There were no differences in LDL-cholesterol, HDL-cholesterol or plasma triglycerides between the groups. Total lipoprotein lipase activity (T-LPL) (LPL + HTGL) of the GAG-PS group at 10 weeks was higher than that of the cholesterol-diet group. These elevated T-LPL levels were mainly due to an increase in the LPL from peripheral tissues. ADP-induced platelet aggregability of the GAG-PS group significantly decreased at 10 weeks when compared to the cholesterol-diet group, and antithrombin-III activity of the GAG-PS group was inversely increased when compared to the cholesterol-diet group. Although there were no differences in aortic levels of total cholesterol and uronic acid between the GAG-PS group and the cholesterol-diet group, the surface involvement of the aorta in the GAG-PS group was significantly lower than that in the cholesterol-diet group. The aortic levels of free cholesterol, hydroxyproline and calcium of the GAG-PS group were significantly decreased when compared to the cholesterol-diet group. These findings suggest that GAG-PS has antiatherosclerotic effects.
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PMID:Effects of polysulfated glycosaminoglycans obtained from bovine lung tissue on hypercholesterolemic rabbits. 239

G protein regulation of human platelet membrane phospholipase A2 activity was investigated at pH 8.0 and 9.0 by studying the effects of the nonhydrolyzable GTP analogue, guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), and of F-/Al3+ ions on arachidonic acid (AA) release. The membrane acted as the source of the enzyme, the substrate, and the G protein. At pH 8.0, 10 and 100 microM GTP gamma S stimulated AA mobilization at least 6-fold. Optimum AA release conditions required 1 mM Ca2+ and 5 mM Mg2+. Nonspecific nucleotide effect was excluded since similar stimulatory effects on AA release were not observed by ATP, GTP, ADP, and NADP. Although at pH 9.0 the GTP gamma S-stimulated AA release was greater than at pH 8.0, it constituted only 26% of the total. At both pH values the effect of F- (10 mM) in the presence of Al3+ (2 microM) was similar to that of GTP gamma S. The G protein inhibitor, guanosine 5'-O-(2-thiodiphosphate), inhibited the GTP gamma S-stimulated AA release by about 80% at pH 8.0 and by 100% at pH 9.0. To determine a possible contribution to AA mobilization by the phospholipase C and diacylglycerol lipase pathway, the effects of neomycin, a phospholipase C inhibitor, were investigated. 100 microM neomycin did not inhibit the GTP gamma S-stimulated AA release at pH 8.0 and only slightly so (17%) at pH 9.0. At pH 8.0 in the presence of Ca2+ the released fatty acids consisted mainly of arachidonic and docosahexaenoic acids (80 and 8%, respectively). GTP gamma S had no effect on the fatty acid profile but only on their quantity. These results provide evidence of G protein regulation of phospholipase A2 activity in isolated platelet membranes.
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PMID:Evidence of GTP-binding protein regulation of phospholipase A2 activity in isolated human platelet membranes. 251 18

The purpose of this study was to characterize the lipolytic activity of the alkaline triglyceride lipase in homogenates of three types of skeletal muscle obtained from heparin-perfused rat hindlimb. Specifically, the red portion of the vastus lateralis, the white portion of the vastus lateralis, and the soleus muscles were examined. To remove capillary-bound lipoprotein lipase from the capillary beds, muscle was perfused with an erythrocyte-free buffer containing 4% albumin, 5 units of heparin/mL, and 7.5 microM adenosine. Adenosine reduced perfusion pressure from 117 +/- 5 to 86 +/- 6 mmHg (1 mmHg = 133.32 Pa), providing evidence for an effective vasodilation. This vasodilation increased the amount of lipoprotein lipase removed from the capillary beds. By the end of the experiment, perfusates were lipoprotein lipase-free. Oxygen supply to the perfused hindlimb appeared adequate as evidenced by similar high energy phosphate values for perfused and contralateral control tissues. For example, in soleus muscle, ATP content was 4.5 +/- 0.6 vs. 4.2 +/- 0.3 mumol/g, ADP concentration was 1.0 +/- 0.2 vs. 1.4 +/- 0.2 mumol/g, and creatine phosphate level was 12.9 +/- 0.7 vs. 11.0 +/- 0.6 mumol/g for perfused and contralateral control soleus, respectively. In addition, K+ output by the hindlimb was negligible, while glycolytic flux of perfused muscle was similar to that measured in control tissue. The findings that triglyceride levels of soleus and red vastus lateralis were decreased suggest that endogenous triglyceride was providing energy for the hindlimb during perfusion. Skeletal muscle triglyceride lipase activity was stimulated by serum and heparin, inhibited by NaCl and protamine, and had a pH optimum of 8.1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of the triacylglycerol lipase activity in three types of rat skeletal muscle. 358 Sep 54

Mono- and diacylglycerol lipases are differentially inhibited by heparin. No other glycosaminoglycan resembles heparin in this respect. Mono- and diacylglycerol lipases can be separated by heparin Sepharose affinity chromatography. Diacylglycerol lipase was completely retained on a heparin--Sepharose column and was eluted with either 0.5 M NaCl or 2-5 mg/ml heparin, whereas monoacylglycerol lipase was recovered in the washings. Adenosine phosphates markedly affected the activity of diacylglycerol lipase in a concentration dependent manner. ATP was the most potent inhibitor followed by ADP. AMP had no effect and cAMP slightly stimulated the diacylglycerol lipase.
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PMID:Separation of bovine brain mono- and diacylglycerol lipases by heparin sepharose affinity chromatography. 647 59

Molecular mechanisms underlying the ability of heparin to enhance the platelet-aggregating effect of various agonists were studied. Heparin potentiates the aggregating effect of adenosine diphosphate (ADP) and epinephrine, but it is uneffective on the aggregation induced by ristocetin and collagen. Heparin inhibits aggregation induced by thrombin in the presence of plasma, but it is uneffective, or sometimes stimulates aggregation, in the absence of plasma. The effects on the platelet-activating factor- (PAF-acether) induced aggregation are very variable. The late phase of the ADP-induced aggregation is sensitive to proteinase inhibitors, but heparin overcomes this inhibitory effect. Drugs which inhibit remodeling of membrane phospholipids abolish the potentiating effect of heparin, while cyclooxygenase inhibitors do not. The proaggregating effect of heparin subfractions correlates with the lipoprotein lipase activity and, slightly, with the molecular weight, but it does not correlate with the anticoagulant activity. Platelets prelabelled with phosphatidyl[U14C]inositol show a very rapid effect of heparin in triggering phosphatidylinositor breakdown and a cooperative effect with ADP, a known agonist of the 'phosphatidylinositol cycle'. Heparin is also effective in stimulating the labelling of polyphosphoinositides in platelets prelabelled with 32Pi. These results, together with the selective sensitivity to drugs, lead to the conclusion that a stimulatory effect on the very early events of remodeling of membrane phospholipids is involved in the platelet proaggregating effect of heparin.
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PMID:Molecular events involved in the proaggregating effect of heparin on human platelets. 649 25

Four healthy men volunteered to be treated for eight to nine months with daily oral levo-norgestrel (250 micrograms) and oral testosterone (200-600 mg) as a possible contraceptive. This was followed by a recovery phase of 5-10 months. The oral steroid combination significantly decreased sperm count in 3 of 4 subjects, and significantly increased abnormal spermatozoa, serum LH was decreased during treatment but serum FSH remained constant, except for one volunteer. Serum testosterone was decreased except for 2 daily peaks associated with the oral testosterone. During the recovery period, sperm counts and morphology, serum testosterone and serum LH returned to normal, whereas serum FSH levels were increased. Platelet aggregability induced by ADP, increased in 3 volunteers during treatment as did fibrinolytic activity and fibrinolytic capacity (2 of 3 subjects). There was a reduction in the hepatic triglyceride lipase activity but no change was seen in serum triglycerides, serum cholesterol, serum LDL, serum HDL, peripheral lipoprotein lipase activity and the intravenous fat tolerance test. No other toxicological side effects were seen.
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PMID:Oral levo-norgestrel - testosterone effects on spermatogenesis, hormone levels, coagulation factors and lipoproteins in normal men. 677 Oct 94

This article reviews the experimental and clinical evidence regarding heparin therapy in the prophylaxis of coronary heart disease. The actions of heparin take place at the vascular endothelium where injected heparin concentrates, and within the bloodstream. At the endothelium heparin acts to prevent endothelial injury, prevent thrombin generation, prevent platelet adhesion to endothelium, and to decrease uptake of serum lipoproteins. Within the bloodstream heparin increases lipoprotein lipase activity and reduces the concentration of atherogenic very low-density lipoproteins. The reduction in lipemia enhances oxygen transfer from blood to the tissues, and decreases thrombin or ADP-induced platelet aggregation. Heparin increases the concentration of high-density lipoproteins. It decreases hypercoagulability and inhibits overactivation of serum complement. Heparin reduced atherosclerosis in most studies in cholesterol-fed animals. In human subjects who had a myocardial infarct at least one year before the onset of treatment, long-term intermittent heparin therapy significantly decreased cardiovascular deaths as compared to control groups.
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PMID:Heparin and atherosclerosis. A review of old and recent findings. 698 41


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