The Lipoprotein Lipase <i>Hin</i> dIII Polymorphism Modulates Plasma Triglyceride Levels in Visceral Obesity

The aim of this study was to investigate the potential interaction between the lipoprotein lipase (LPL) Hin dIII polymorphism and visceral adipose tissue (AT) accumulation in the modulation of triglyceride levels in visceral obesity. The LPL- Hin dIII genotype was determined by polymerase chain reaction in 52 men. Twenty-three subjects were heterozygous (+/−) and 28 were homozygous (+/+) for the presence of the restriction site. One subject who was homozygous for the − allele was excluded from analysis. Body mass index (BMI), fasting insulin level, and visceral AT area as measured by computed tomography were positively correlated with triglyceride levels only in subjects homozygous for the + allele. Furthermore, whereas these variables were negatively correlated with plasma HDL 2 cholesterol concentrations in the +/+ group, these associations were not found in +/− heterozygotes, with the exception of BMI. To further investigate the interaction of the LPL- Hin dIII polymorphism with visceral obesity and hyperinsulinemia, the two genotype groups were further subdivided on the basis of BMI (low versus high), fasting insulin level (low versus high), and visceral AT area (low versus high), and their lipoprotein profiles were compared. Elevated levels of abdominal visceral AT were significantly associated with increased triglyceride concentrations in +/+ homozygous men, suggesting that visceral obesity may lead to hypertriglyceridemia in the presence of the +/+ genotype. In the +/− group, variation in the amount of visceral AT was not associated with differences in triglyceride concentration. However, hypertriglyceridemia and an increased cholesterol-to–HDL cholesterol ratio were observed in the hyperinsulinemic state irrespective of LPL- Hin dIII genotype status. Finally, similar positive correlations were observed between visceral AT accumulation and plasma insulin level in the homozygous (+/+) and heterozygous (+/−) groups, suggesting that the hyperinsulinemic–insulin-resistant state that is frequently associated with visceral obesity is independent of LPL- Hin dIII genotype. These results suggest that the Hin dIII polymorphism may modulate the magnitude of the dyslipidemic state associated with visceral obesity.