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Variations in high‐density lipoprotein cholesterol in relation to physical activity and Taq 1B polymorphism of the cholesteryl ester transfer protein gene
Author(s) -
Mukherjee M,
Shetty KR
Publication year - 2004
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.0009-9163.2004.0237.x
Subject(s) - cholesterylester transfer protein , medicine , endocrinology , cholesterol , genotype , lipoprotein , high density lipoprotein , coronary artery disease , morning , gene polymorphism , biology , gene , genetics
The aim of the study was to determine any association of physical activity and Taq 1B polymorphism in the cholesteryl ester transfer protein gene on high‐density lipoprotein (HDL) cholesterol. Five hundred and four subjects, 390 males and 114 females consisting of an equal number of age‐ and sex‐matched healthy controls and patients with coronary artery disease, were included. The mean age (±SD) of the patients and controls were 57.5 ± 10.6 years and 56.8 ± 11.0 years, respectively. All the patients underwent coronary angiography; 33, 58, 63, and 98 patients had normal coronaries, single‐, two‐, or triple‐vessel disease, respectively. A third of the patients had suffered from a myocardial infarction. The genotype distribution conforming to Hardy–Weinberg equilibrium was similar for cases and controls. The mean HDL cholesterol increased from B1B1 through B2B2 genotype in controls and sedentary male patients. Self‐reported leisure time physical activity, consisting mostly of an hour of morning walk daily, was associated with a rise in mean HDL cholesterol in male controls (33.6 ± 7.9 mg/dl to 36.2 ± 8.9 mg/dl, p = 0.037) and patients (32.4 ± 7.9 mg/dl to 35.7 ± 11.0 mg/dl; p = 0.018). The exercise‐associated rise in HDL cholesterol was most pronounced in controls (32.1 ± 9.1 mg/dl to 36.8 ± 9.3 mg/dl, p = 0.05) and male patients (30.5 ± 7.4 mg/dl to 37.2 ± 9.7 mg/dl, p = 0.007) with B1B1 rather than B1B2 or B2B2 genotype. The results suggest a possible gene‐environment interaction in the regulation of HDL cholesterol that needs to be confirmed in other populations and larger samples to rule out a chance occurrence.