Vol 9, No 1 (2005)
Original paper
Published online: 2005-02-04
HindIII polymorphism of the lipoprotein lipase gene and blood pressure, anthropometric measurements, carotid artery structure and selected indices of the metabolism of glucose and lipids - family study
Nadciśnienie tętnicze 2005;9(1):11-21.
Abstract
Background The prevalence of the metabolic syndrome, which includes essential hypertension, is continuously increasing. The aim of the study was to evaluate the influence
of the lipoprotein lipase (LPL) gene HindIII polymorphism on blood pressure (BP), obesity, fasting glucose
and lipoprotein profile, as well as carotid intima-media thickness (IMT) in the cohort of Polish families.
Material and methods We genotyped 326 subjects, members of 86 nuclear families, enrolled in the populationbased study, for the HindIII polymorphism of the LLP gene. We excluded from this analysis 15 subjects with diabetes mellitus. Remaining 311 persons underwent conventional BP measurement during two separate home visits, 5 times on each visit. Anthropometric data were collected with standardized protocol. Peripheral blood was sampled in fasting subjects for routine biochemistry, including glucose and lipoprotein profile. Carotid IMT measured by carotid ultrasound was used as an index of atherosclerosis.
Results Genotype frequencies were 55.0% for +/+, 36.7% for +/– and 8.3% for –/–, and did not deviate from the Hardy-Weinberg equilibrium (p = 0.44). Among parents (mean age: 50.7 years) –/– homozygotes as compared to (+) allele carriers showed increased body mass index (31.6 vs. 28.0 kg/m2; p = 0.01) and increased total cholesterol (6.23 vs. 5.56 mmol/l; p = 0.05). Parents homozygous for (–) allele presented also tendency towards higher levels of LDL cholesterol (3.92 vs. 3.29 mmol/l; p = 0.06) and carotid IMT (0.87 vs. 0.71 mm; p = 0.09). In offspring generation (mean age: 24.1 years), carrying of (–) allele resulted in higher fasting glucose (4.48 vs. 4.12 mmol/l; p = 0.003), total cholesterol (4.71 vs. 4.37 mmol/l; p = 0.01) and LDL cholesterol (2.58 vs. 2.33 mmol/l; p = 0.04). In quantitative transmission disequillibrium test, HindIII polymorphism of LPL mainly influenced fasting glucose levels (chi2 = 6.62, p = 0.01).
Conclusions HindIII polymorphism of the lipoprotein lipase gene influences lipids metabolism in both generations and in offspring generation also glucose metabolism. In parents generation, it is also related to obesity and increased carotid IMT.
Material and methods We genotyped 326 subjects, members of 86 nuclear families, enrolled in the populationbased study, for the HindIII polymorphism of the LLP gene. We excluded from this analysis 15 subjects with diabetes mellitus. Remaining 311 persons underwent conventional BP measurement during two separate home visits, 5 times on each visit. Anthropometric data were collected with standardized protocol. Peripheral blood was sampled in fasting subjects for routine biochemistry, including glucose and lipoprotein profile. Carotid IMT measured by carotid ultrasound was used as an index of atherosclerosis.
Results Genotype frequencies were 55.0% for +/+, 36.7% for +/– and 8.3% for –/–, and did not deviate from the Hardy-Weinberg equilibrium (p = 0.44). Among parents (mean age: 50.7 years) –/– homozygotes as compared to (+) allele carriers showed increased body mass index (31.6 vs. 28.0 kg/m2; p = 0.01) and increased total cholesterol (6.23 vs. 5.56 mmol/l; p = 0.05). Parents homozygous for (–) allele presented also tendency towards higher levels of LDL cholesterol (3.92 vs. 3.29 mmol/l; p = 0.06) and carotid IMT (0.87 vs. 0.71 mm; p = 0.09). In offspring generation (mean age: 24.1 years), carrying of (–) allele resulted in higher fasting glucose (4.48 vs. 4.12 mmol/l; p = 0.003), total cholesterol (4.71 vs. 4.37 mmol/l; p = 0.01) and LDL cholesterol (2.58 vs. 2.33 mmol/l; p = 0.04). In quantitative transmission disequillibrium test, HindIII polymorphism of LPL mainly influenced fasting glucose levels (chi2 = 6.62, p = 0.01).
Conclusions HindIII polymorphism of the lipoprotein lipase gene influences lipids metabolism in both generations and in offspring generation also glucose metabolism. In parents generation, it is also related to obesity and increased carotid IMT.
Keywords: blood pressurecarotid intima-media thicknessmetabolic syndromelipoprotein lipasepolymorphism