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Volume 146, Issue 1, Pages 153-160 (September 1999)


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Absence of association between genetic variation in the LIPC gene promoter and plasma lipoproteins in three Canadian populations

Robert A HegeleaCorresponding Author Informationemail address, Stewart B Harrisb, J Howard Bruntc, T Kue Youngd, Anthony J.G Hanleye, Bernard Zinmaneg, Philip W Connellyfgh

Received 27 July 1998; received in revised form 17 February 1999; accepted 23 February 1999. published online 16 August 2004.

Abstract 

The promoter sequence variant -480T in the hepatic lipase gene (LIPC) has been shown to be significantly associated with low post-heparin hepatic lipase activity. Some studies have also found that the -480T variant is associated with elevation in plasma HDL cholesterol. We tested for associations of LIPC -480T with plasma lipoprotein traits in samples taken from three distinct Canadian populations: 657 Alberta Hutterites, 328 Ontario Oji-Cree and 210 Keewatin Inuit. Plasma HL activity was not available for analyses. The LIPC -480T allele frequencies in these three groups, respectively, were 0.219, 0.527 and 0.383, and the prevalence of LIPC -480T/T homozygotes was, respectively, 0.042, 0.274 and 0.167. No significant association was found between LIPC -480T and plasma HDL cholesterol or apolipoprotein AI concentration, after adjusting for covariates including gender and body mass index. There was no consistent relationship between the population mean plasma HDL cholesterol concentration and the population LIPC -480T frequency. Our findings are consistent with the idea that the common promoter variation in LIPC, which has been reported to be associated with variation in post heparin HL activity and HDL triglyceride concentration, is not always associated with variation in plasma HDL cholesterol concentration, possibly due to yet unspecified environmental or genetic factors.

a Blackburn Cardiovascular Genetics Laboratory, Robarts Research Institute, Department of Medicine, 406-100 Perth Drive, London, Ont., N6A 5K8, Canada

b Thames Valley Family Practice Research Unit, University of Western Ontario, London, Ont., Canada

c School of Nursing, University of Victoria, Victoria, BC, Canada

d Northern Health Research Unit, Department of Community Health Sciences, University of Manitoba, Winnipeg, Man., Canada

e Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ont., Canada

f St. Michael’s Hospital, Toronto, Ont., Canada

g Department of Medicine, University of Toronto, Toronto, Ont., Canada

h Department of Biochemistry, University of Toronto, Toronto, Ont., Canada

Corresponding Author InformationCorresponding author. Tel.: +1-519-6633461; fax: +1-519-6633789

PII: S0021-9150(99)00113-6


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