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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:714-720.)
© 1995 American Heart Association, Inc.

Articles

The Lipoprotein Lipase HindIII Polymorphism Modulates Plasma Triglyceride Levels in Visceral Obesity

Marie-Claude Vohl; Benoît Lamarche; Sital Moorjani; Denis Prud'homme; André Nadeau; Claude Bouchard; Paul-J. Lupien; Jean-Pierre Després

From the Lipid Research Center, CHUL Research Center (M.-C.V., B.L., S.M., P.-J.L., J.-P.D.), the Physical Activity Sciences Laboratory (D.P., C.B.), and the Diabetes Research Unit, CHUL Research Center (A.N.), Laval University, Ste-Foy, Québec.

Correspondence to Dr Jean-Pierre Després, Lipid Research Center CHUL, 2705 Laurier Blvd, Québec, GIV 4G2, Canada.

Abstract The aim of this study was to investigate the potential interaction between the lipoprotein lipase (LPL) HindIII polymorphism and visceral adipose tissue (AT) accumulation in the modulation of triglyceride levels in visceral obesity. The LPL-HindIII 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 HDL₂ 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-HindIII 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-HindIII 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-HindIII genotype. These results suggest that the HindIII polymorphism may modulate the magnitude of the dyslipidemic state associated with visceral obesity.

Key Words: lipoprotein lipase • visceral obesity • insulin • hypertriglyceridemia • candidate genes

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