HindIII DNA polymorphism in the lipoprotein lipase gene and plasma lipid phenotypes and carotid artery atherosclerosis |
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Authors: | Ling Chen Wolfgang Patsch E Boerwinkle |
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Institution: | (1) Human Genetics Center, University of Texas Health Science Center, Houston TX 77225, USA Tel.: +1-713-792-4680; Fax: +1-713-792-4615; e-mail eboerwin@gsbs.gs.uth.tmc.edu, US;(2) Department of Laboratory Medicine, Landeskrankenanstalten Salzburg, A-5020, Salzburg Austria, AT |
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Abstract: | Lipoprotein lipase (LPL) is the rate limiting enzyme in the hydrolysis of core triglyceride in chylomicron and very low density
lipoprotein (VLDL) thus affecting a broad spectrum of plasma lipid levels. In this paper, we investigated the association
of a HindIII polymorphism in the LPL gene with plasma lipid levels and carotid artery wall thickness measured by B-mode ultrasonography.
A total of 238 Caucasian subjects were selected from the Atherosclerosis Risk In Community (ARIC) study (male = 131, female
= 107) based on their fasting triglyceride and LDL-cholesterol levels: normolipidemic (n = 48), hypertriglyceridemic (n = 44), hypercholesterolemic (n = 36), and hypertriglyceridemic-hypercholesterolemic (n = 110) groups. We observed a marginally significant association between lipid phenotypes and HindIII genotypes (P = 0.04) in males, with the hypertriglyceridemic and hypercholesterolemic groups having a higher frequency (0.65) of the H+H+
genotype than the other two groups (pooled: 0.55). In males, there was also a significant association between HindIII genotypes and carotid artery wall thickness after considering the effects of age, body mass index, cigarette smoking,
lipid phenotype and diabetes status (P = 0.013), with the H+H+ genotype having a higher average value of carotid artery wall thickness (0.84 ± 0.15 mm) than the
other two genotype groups (0.76 ± 0.14 mm in H+H– genotype class, 0.75 ± 0.13 mm in H–H– genotype class). In females, no significant
associations among LPL HindIII genotype, lipid phenotype and carotid artery wall thickness were observed. These results suggest that the LPL HindIII polymorphism influences LPL-catalyzed, triglyceride-rich lipoprotein metabolism and carotid artery atherosclerosis in
a gender-specific manner.
Received: 28 December 1995 / Revised: 2 May 1996 |
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