title: HindIII DNA polymorphism in the lipoprotein lipase gene and plasma lipid phenotypes and carotid artery atherosclerosis.
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 = 1.31, 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.
authors.affiliation: Human Genetics Center, University of Texas Health Science Center, Houston 77225, USA.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: W
authors.initials: W
authors.lastname: Patsch
authors.forename: E
authors.initials: E
authors.lastname: Boerwinkle
mesh_terms: D000328:Adult; D000428:Alcohol Drinking; D001161:Arteriosclerosis / Q000235:genetics*; D015992:Body Mass Index; D002339:Carotid Arteries; D002784:Cholesterol / Q000097:blood; D004247:DNA; D015247:Deoxyribonuclease HindIII; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000150:complications; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011110:Polymorphism, Genetic; D012907:Smoking; D014280:Triglycerides / Q000097:blood
chemical_list: D008055:Lipids; D014280:Triglycerides; D004247:DNA; D002784:Cholesterol; D008071:Lipoprotein Lipase; D015247:Deoxyribonuclease HindIII