Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A protein kinase inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) increased lipoprotein lipase (LPL) activity in isolated rat fat pads in a time- and dose-dependent manner. The incubation of H-7 with partially purified LPL did not affect its activity. Under the marked inhibition of protein synthesis by cycloheximide, H-7 still showed a full effect on the increase in LPL activity. A slight but significant increase in LPL activity in the fat pads was observed with inhibitors of cyclic nucleotide-dependent protein kinase. H-7, therefore, may increase LPL activity through processes other than the direct activation of the LPL molecule, or the stimulation of LPL molecule synthesis; probably through a decrease in the activity of protein kinases, especially protein kinase C.
Chem Pharm Bull (Tokyo) 1991 Sep
PMID:Protein kinase inhibitor H-7 increases lipoprotein lipase activity in isolated rat fat pads. 180 58

Earlier studies have shown that bradykinin stimulated release of catecholamines from chromaffin cells by an influx of calcium through dihydropyridine-insensitive channels, and also that bradykinin stimulated (poly)phosphoinositide hydrolysis. To investigate membrane-bound second messengers in chromaffin cells, and to elucidate any role these may play in stimulus-secretion coupling, we have studied the influence of bradykinin on diacylglycerol and phosphatidic acid (PA). Using equilibrium labelling of primary cultures of chromaffin cells with [3H]arachidonic acid or [3H]glycerol, we found no influence of bradykinin (10 nM) on labelled diacylglycerol formation, either in the presence or absence of inhibitors of diacylglycerol lipase or kinase. However, when we used cells prelabelled with 32Pi for 2.5 h, we found that bradykinin produced a substantial stimulation of label found in PA, with an EC50 value of about 1 nM. This bradykinin stimulation of [32P]PA formation was only partially dependent on extracellular calcium, in contrast to the smaller response to nicotine, which was completely dependent on extracellular calcium. Short (10 min) pretreatment with tetradecanoylphorbol acetate (TPA) almost completely eliminated the bradykinin-stimulated formation of inositol phosphates, but failed to affect bradykinin stimulation of label in PA, suggesting that PA production in response to bradykinin is not downstream of phospholipase C activation. TPA alone failed to stimulate [32P]PA substantially, whereas long-term (24 or 48 h) treatment with TPA failed to attenuate the response to bradykinin. Diacylglycerol kinase inhibitors were also without effect on the bradykinin stimulation of [32P]PA. These results suggest that bradykinin stimulates PA production by a mechanism independent of the activation of protein kinase C.(ABSTRACT TRUNCATED AT 250 WORDS)
J Neurochem 1991 Sep
PMID:Influence of bradykinin on diacylglycerol and phosphatidic acid accumulation in cultured bovine adrenal chromaffin cells. 186 Nov 47

Coffee consumption has been associated with elevated plasma cholesterol. One hundred eighty-one men consumed a standard caffeinated coffee for 2 mo followed by randomization to continue caffeinated coffee (control), change to decaffeinated coffee or no coffee for 2 mo. Plasma low-density-lipoprotein (LDL) cholesterol and apolipoprotein B concentrations increased significantly (0.12 +/- 0.65 mmol/L, P less than 0.025; 0.06 +/- 0.12 g/L, P less than 0.0004, respectively) in the group that changed to decaffeinated coffee. In a subgroup (n = 51), post-heparin lipoprotein lipase decreased significantly more (-270 mmol free fatty acids.L-1.h-1, P less than 0.003) in the decaffeinated-coffee group. Resting heart rate and blood pressure did not change significantly. Change from caffeinated to decaffeinated coffee increased plasma LDL cholesterol and apolipoprotein B whereas discontinuation of caffeinated coffee revealed no change. This finding suggests that a coffee component other than caffeine is responsible for the LDL cholesterol, apolipoprotein B, and lipase activity changes reported in this investigation.
Am J Clin Nutr 1991 Sep
PMID:Caffeinated and decaffeinated coffee effects on plasma lipoprotein cholesterol, apolipoproteins, and lipase activity: a controlled, randomized trial. 150 76

In avian-cultured adipocytes 76% of the newly synthesized lipoprotein lipase is degraded before release into the medium (Cupp, M., Bensadoun, A., and Melford, K. (1987) J. Biol. Chem. 262, 6383-6388). The same group (Cisar, L. A., Hoogewerf, A. J., Cupp, M., Rapport, C. A., and Bensadoun, A. (1989) J. Biol. Chem. 264, 1767-1774) has proposed that the interaction of lipoprotein lipase with a class of cell surface heparan sulfate proteoglycans is necessary for degradation to occur. To test further this hypothesis, the binding capacity of the plasma membrane for the lipase was decreased by inhibiting the sulfation of glycosaminoglycans with sodium chlorate, an inhibitor of sulfate adenyltransferase. Chlorate decreased sulfate incorporation into trypsin-releasable heparan sulfate proteoglycans to 20% of control levels. The amount of uronic acid in the trypsin-releasable heparan sulfate proteoglycans remained constant. Therefore, chlorate decreased sulfation density on heparan sulfate chains by approximately 5-fold. In the same fractions, chlorate increased the median heparan sulfate Mr measured on Sephacryl S-300. Chlorate decreased the maximum binding of 125I-lipoprotein lipase to adipocytes by 4-fold, but no significant effects on the affinity constants were observed. Chlorate increased lipoprotein lipase secretion in a dose-dependent relationship up to 30 mM. Utilizing a pulse-chase protocol, it was shown that lipase synthesis in control and chlorate-treated cells was not significantly different and that the increased secretion could be accounted for by a decreased lipoprotein lipase degradation rate. In control cells 77 +/- 11% of the synthesized enzyme was degraded whereas in chlorate-treated cells degradation was reduced to 42 +/- 9% of the synthesized amount. The present study shows that decreased sulfation of heparan sulfate proteoglycans decreases the maximum binding of the lipase for the adipocyte cell surface. Consistent with the model that binding of lipoprotein lipase to cell surface heparan sulfate is required for lipase degradation, degradation is reduced in chlorate-treated cultures. In this report it is also shown that chlorate inhibits lipoprotein lipase sulfation and that desulfation of the enzyme has no effect on its catalytic efficiency or on its binding to cultured adipocytes.
J Biol Chem 1991 Sep 05
PMID:Effect of chlorate on the sulfation of lipoprotein lipase and heparan sulfate proteoglycans. Sulfation of heparan sulfate proteoglycans affects lipoprotein lipase degradation. 188 87

Our primary aim was to determine the extent to which intraplasmic retinyl palmitate (RP) transfers to other lipoprotein particles when chylomicron remnants are not produced and/or the plasma RP residence time is increased. The study was conducted on three familial type I hyperlipoproteinemic patients, four lipoprotein lipase (LpL)-deficient heterozygotes, and three controls on a metabolic research unit. To each subject, a fat load was administered containing 16% of total daily calories in type I patients, 40% in heterozygotes and controls, plus 60,000 U/m2 vitamin A. Triglyceride (TG) and RP levels were evaluated in chylomicron and nonchylomicron fractions. Delay in the clearance of chylomicron fraction RP and the marked deficiency in nonchylomicron-RP (presumed lack of remnant production) in all three type I patients suggests that RP does not demonstrate significant intraplasmic transfer from chylomicrons to existent apolipoprotein B100 particles. In contrast to noncoincident TG and RP peaking in the normal subject, heterozygotes were found to demonstrate coincident plasma TG and RP curves, which is consistent with a common catabolic pathway for both TG and RP and inconsistent with intraplasmic RP transfer. This corroborates reports on compromised chylomicron clearance in heterozygotes. We conclude that RP is an appropriate representative marker for intestinally derived particles in LpL-deficient or partially deficient individuals.
J Clin Invest 1991 Sep
PMID:Chylomicron-retinyl palmitate clearance in type I hyperlipidemic families. 188 83

Very-low-density lipoprotein triglyceride (VLDL-TG) catabolism was studied in rats receiving either fructose or glucose as a 10% drinking solution. Consumption of either of the hexoses for 16 hours significantly elevated postheparin plasma (PHP) lipoprotein lipase (LPL) activity compared with normal control animals. Prolonged feeding of the carbohydrates for 14 days abolished the higher LPL activities, which were similar to control levels. PHP hepatic lipase (HL) activity was significantly reduced in carbohydrate-fed rats compared with control animals despite the duration of feeding. The kinetic parameters Km and Vmax cannot be obtained with lipoproteins and so the first-order rate constant (k1) of triglyceride hydrolysis was used to assess the effectiveness of VLDL-TG as substrates for endothelial lipases. VLDL-TG from fructose and VLDL-TG from glucose donors was lipolyzed with PHP LPL and HL from normal rats. The k1 (fraction of VLDL-TG lipolyzed) of VLDL-TG was found to be lower when donors had been fed fructose compared with VLDL that had come from glucose-fed donors. Rates of VLDL-TG removal from fructose and glucose donors were determined simultaneously in perfused livers of normal control, fructose-fed, and glucose-fed animals. Livers of fructose-fed animals cleared VLDL-TG at a slower rate than livers from glucose-fed or control rats. VLDL-TG from fructose-fed rats was cleared less effectively than VLDL-TG from glucose-fed rats in livers of both control and glucose-fed animals. We conclude that an impairment in the ability of fructose-fed rats to hydrolyze VLDL-TG, and of their livers to remove VLDL-TG, may in part explain fructose-induced hypertriglyceridemia.
Metabolism 1991 Sep
PMID:Partial characterization of the fructose-induced defect in very-low-density lipoprotein triglyceride metabolism. 189 53

1. The possible prediction of fatness in 6-week-old broiler chickens was examined by measuring lipoprotein lipase (LPL) activity and lipid content in the abdominal adipose tissue. 2. Fat pad weight, as representing the degree of fatness in broiler chickens, was moderately well correlated (r = 0.54) with lipid content (g/100 g pad) and negatively correlated with LPL activity (r = 0.13). 3. It was concluded that the measurement of lipid content in samples from adipose tissue can be indicative of fatness of birds, while enzymic measurements are less valuable.
Br Poult Sci 1991 Sep
PMID:The possible prediction of fatness in broiler chickens by biochemical measurements on adipose tissue. 193 48

Two experiments were performed to determine whether esterification is a major pathway of fatty acid utilization within porcine placenta and to determine what metabolic parameters may limit fatty acid transfer to the fetal pig. Maternal (endometrium) and fetal (chorioallantois) placenta were obtained by Caesarean section at d 110 of gestation in both experiments. Eight gilts were used in the first experiment. Tissue sections were incubated with palmitate at concentrations ranging from .25 to 2.0 mM. Maternal placenta metabolized palmitate at a higher rate than fetal placenta, although fetal placenta was more efficient in esterifying palmitate. Esterification composed the majority of palmitate utilization within fetal and maternal placenta. The second experiment evaluated the effect of dietary lipid on placental fatty acid metabolism and evaluated the ability of placenta to mobilize lipids. Fourteen gilts were divided into two groups of seven and fed a diet containing 15% tallow diet or a diet not supplemented with tallow (control) from d 90 to 110 of gestation. Dietary lipid had no detectable effects on lipoprotein lipase activity, [14C]palmitate metabolism, or lipolysis by the maternal or fetal placenta. Lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic activity of placental tissues was minimally affected by incubation with various proposed lipolytic agents. The data indicate that supply of fatty acids to the fetal pig may be limited by transfer of plasma fatty acids into the cytoplasm of placental cells or by regulatory enzymes for intermediate esterification; both types of limitations have been proposed to be influenced by fatty-acid binding proteins.
J Anim Sci 1991 Sep
PMID:Fatty acid metabolism by the porcine placenta. 193 47

Improved reproductive performance and reduced incidence of metabolic disorders have been postulated to be benefits of feeding supplemental fat to dairy cows. Increased plasma nonesterified fatty acid concentrations during fat supplementation may result from incomplete tissue uptake of fatty acids after lipoprotein lipase hydrolysis of very-low-density lipoprotein triglyceride; however, evidence suggests that net adipose tissue triglyceride hydrolysis may be increased during fat supplementation. Plasma 3-OH-butyrate concentrations remain relatively constant during fat supplementation but may have a tendency to be reduced if fat is supplemented to cows having relatively high basal plasma 3-OH-butyrate concentrations. Because plasma ketone levels usually increase when nonesterified fatty acid concentrations are elevated, it is hypothesized that potential antiketogenic effects of added fat are due to a glucose sparing effect. Supplemental fat does not seem to reduce hepatic lipid infiltration near the time of calving. Potential mechanisms by which supplemental fat may improve reproductive performance include stimulation of prostaglandin F2 a synthesis and secretion and enhanced utilization of blood cholesterol for progesterone synthesis. Days postpartum until first ovulation and luteal function of dairy cattle have been related to energy balance during the first 3 wk postpartum. Energy balance data for early lactation cows fed supplemental fat are not plentiful; however, slight but statistically nonsignificant increases have been observed when feeding fat. Cows fed supplemental fat that experience improved energy balance may begin to cycle sooner because of enhanced follicular growth and development. Applied studies examining the effects of supplemental fat on reproductive performance have provided inconsistent results.
J Anim Sci 1991 Sep
PMID:Effects of dietary fat on metabolic disorders and reproductive performance of dairy cattle. 193 63

Abnormalities of plasma lipid and lipoprotein concentrations are common in both insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In general, individuals with IDDM who are untreated or inadequately treated have elevations in both postprandial and fasting triglyceride levels in association with reduced activity of lipoprotein lipase. Low-density lipoprotein (LDL) cholesterol levels can rise when insulin deficiency impacts on LDL-receptor function. When patients with IDDM are treated and plasma glucose levels well controlled, plasma very-low-density lipoprotein (VLDL) triglyceride and LDL cholesterol levels are usually normal. In addition, plasma high-density lipoprotein (HDL) cholesterol levels are normal or elevated in well-controlled IDDM subjects. In NIDDM, increased VLDL triglyceride and reduced HDL cholesterol concentrations are common and are only partially related to glycemic control. Overproduction of VLDL leads to hypertriglyceridemia, which can be exacerbated if lipoprotein lipase activity is also reduced. The regulation of LDL levels is complex; catabolism can be reduced if significant insulin deficiency exists or increased if significant hypertriglyceridemia is present. The reduced levels of HDL cholesterol in NIDDM appear to be related to increased exchange of HDL cholesteryl esters for VLDL triglycerides, although other mechanisms may exist. The roles of insulin resistance, obesity, and independently inherited abnormalities of lipoprotein metabolism in the etiology of dyslipidemia of NIDDM are complex and require further investigation. Finally, the effects of diabetes on glycosylation of apoproteins; on other lipid enzymes, particularly hepatic triglyceride lipase; on lipoprotein surface lipids; and on hepatic uptake of remnants have only just begun to be defined. In view of the marked increase in atherosclerotic cardiovascular disease in individuals with diabetes mellitus, prompt attention to and aggressive therapy for dyslipidemia should be a central component of care for these patients.
Diabetes Care 1991 Sep
PMID:Lipoprotein physiology in nondiabetic and diabetic states. Relationship to atherogenesis. 195 76


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>