Common C-to-T Substitution at Position −480 of the Hepatic Lipase Promoter Associated With a Lowered Lipase Activity in Coronary Artery Disease Patients

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Abstract
Abstract We studied the molecular basis of low hepatic lipase (HL) activity in normolipidemic male patients with angiographically documented coronary artery disease (CAD). In 18 subjects with a lowered HL activity (P =.035). In the CAD patients, the C-to-T substitution was associated with a lowered lipase activity (heterozygotes −15%, homozygotes −20%). The patients were divided into quartiles on the basis of HL activity. Sixty percent (allele frequency 0.32) of the patients in the lowest quartile (HL activity 466 mU/mL). In the noncarriers, but not in the carriers, HL activity was related with plasma insulin, being increased at higher insulin concentration. Homozygous carriers had a significantly higher HDL cholesterol level than noncarriers (1.13±0.28 mmol/L versus 0.92±0.22 mmol/L, P <.02). Our results show that a C-to-T substitution at −480 of the HL promoter is associated with a lowered HL activity. The base substitution, or a closely linked gene variation, may contribute to the variation in HL activity and affect plasma lipoprotein metabolism.

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