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)

In an earlier study it was shown that retinyl palmitate appeared to be a satisfactory label for the core of chylomicrons and their remnants. When chylomicrons were endogenously labeled with retinyl palmitate and pulse-injected into healthy donors, retinyl palmitate was cleared from plasma by a first order process. Its fractional decay constant was very similar to the fractional catabolic rate of VLDL triglycerides, a lipoprotein lipase-dependent process, and 2-3 times slower than hepatic chylomicron remnant uptake in experimental animals. We, therefore, investigated whether plasma clearance of retinyl palmitate-labeled chylomicrons is accelerated by enhanced plasma triglyceride hydrolysis produced by heparin administration. Five healthy subjects took retinyl palmitate by mouth and 5-6 hr later two units of plasma were obtained by plasma-pheresis. After storage for 42 hr, the units were pooled and separated into two equal volumes. The first half was injected into the donor and plasma retinyl palmitate and chylomicron triglyceride were measured for 3.5 hr (control study). Heparin was then given intravenously as a bolus followed by an infusion for 7 hr. A second retinyl palmitate clearance (postheparin study) was performed during the heparin infusion. Plasma lipolytic activity and retinyl palmitate and chylomicron triglyceride concentrations were measured serially. Total plasma lipolytic activity and hepatic triglyceride lipase activity were increased approximately 500-fold during postheparin studies, enhancing triglyceride decay 2.5- to 3-fold. Retinyl palmitate plasma decay, however, was unaffected. Retinyl palmitate plasma decay was a biexponential concentration-dependent function in eighty of ten pre- and postheparin studies with the first, rapid exponential accounting for 90 +/- 4% of total plasma retinyl palmitate decay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma decay of chylomicron remnants is not affected by heparin-stimulated plasma lipolytic activity in normal fasting man. 403 63

The effect of gemfibrozil on postprandial lipoprotein metabolism was investigated in a 12-week, randomized, double-blind, placebo-controlled trial in 20 non-insulin-dependent diabetic patients with moderate hypertriglyceridemia. The patients were given a meal containing 78 g of fat and 345,000 units of vitamin A to label chylomicrons and their remnants. Plasma obtained at various times during the fat-load test was separated into six fractions by gradient-density ultracentrifugation. Gemfibrozil reduced the postprandial triglyceride response, measured as the area under the time-dependent concentration curve, on average by 32% in whole plasma, by 38% in the Svedberg flotation unit (Sf) 1,100-3,200 chylomicron fraction, by 36% in Sf 400-1,100 chylomicrons, and by 38% in the Sf 60-400 lipoproteins. Retinyl palmitate, a measure of intestinally derived particles, was reduced in plasma by 34%, in Sf 1,100-3,200 by 46%, in Sf 400-1,100 by 44%, and in Sf 60-400 by 37%. All these reductions were significant in comparison with the placebo group. Particles with Sf < 60 were not significantly affected. In contrast to earlier observations in healthy subjects, no significant negative correlations existed between postprandial lipemia and high density lipoprotein cholesterol or the postheparin lipoprotein lipase activity. The reduction of the potentially atherogenic chylomicron remnants may decrease the risk of atherosclerosis in non-insulin-dependent diabetes mellitus, a hypothesis that awaits testing in prospective studies.
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PMID:Gemfibrozil reduces postprandial lipemia in non-insulin-dependent diabetes mellitus. 842 63

The lipoprotein lipase (LPL) promoter -93T/G transition has previously been reported as having a triglyceride (Tg)-lowering effect, whereas the D9N variant has been shown to have a Tg-raising effect. These two variants were studied in 66 healthy subjects of Hispanic and 42 subjects of African-American origin, who had participated in a study of postprandial lipemia. While the allele frequency of the -93G was significantly different in the Hispanics and African Americans (0.09: 95% CI 0.04-0.13 and 0.28: 95% CI 0.19-0.38; P=0.0001, respectively), the N9 allele frequency was not different (0.06: 95% CI 0.02-0.1 and 0.05: 95% CI 0.002-0.093, respectively). Linkage disequilibrium between the -93T/G and D9N was highly significant in Hispanics (delta=0.67. P=0.0001), compared to delta=0.09 (NS) in African-Americans. In the combined group, compared to individuals with the common genotype (TT/DD; n=71) with fasting plasma Tg of 1.34 (+/-4.5% SEM) mmol/l, carriers of the G/D haplotype (TG/DD + GG/DD; n=25) had significantly lower plasma Tg levels of 1.08 (+/-10% SEM) mmol/l (P < 0.02). After the fat meal, compared to individuals with neither mutation, TT/DD, the effect of the G/D haplotype was to reduce significantly postprandial Tg (P < 0.036). Retinyl palmitate concentration at 5 hrs was significantly lower in G/D carriers than TT/DD individuals (P < 0.05). The lipid-raising effect of the N9 allele in carriers of the -93G (TG/DN + GG/DN) and effect on postprandial Tg clearance was not significant in this group. Thus carriers of the G/D haplotype have lower fasting plasma Tg and reduced alimentary lipemia. This allele may be associated with reduced risk of coronary artery disease.
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PMID:LPL promoter -93T/G transition influences fasting and postprandial plasma triglycerides response in African-Americans and Hispanics. 964 50