L. Chen et al., HINDIII DNA POLYMORPHISM IN THE LIPOPROTEIN-LIPASE GENE AND PLASMA-LIPID PHENOTYPES AND CAROTID-ARTERY ATHEROSCLEROSIS, Human genetics, 98(5), 1996, pp. 551-556
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 t
he 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 LD
L-cholesterol levels: normolipidemic (n = 48), hypertriglyceridemic (n
= 44), hypercholesterolemic (n = 36), and hypertriglyceridemic-hyperc
holesterolemic (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 group
s 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 ass
ociation between HindIII genotypes and carotid artery wall thickness a
fter considering the effects of age, body mass index, cigarette smokin
g, lipid phenotype and diabetes status (P = 0.013), with the H+H+ geno
type 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 f
emales, no significant associations among LPL HindIII genotype, lipid
phenotype and carotid artery wall thickness were observed. These resul
ts suggest that the LPL HindIII polymorphism influences LPL-catalyzed,
triglyceride-rich lipoprotein metabolism and carotid artery atheroscl
erosis in a gender-specific manner.