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Genetic variation in LMNA modulates plasma leptin and indices of obesity in aboriginal Canadians

¹ John P. Robarts Research Institute
² Centre for Studies in Family Medicine, University of Western Ontario, London, Ontario N6A 5K8
³ Samuel Lunenfeld Research Institute and Department of Medicine, Mount Sinai Hospital, University of Toronto, Ontario, Canada M5G 1X5

Hegele, Robert A., Henian Cao, Stewart B. Harris, Bernard Zinman, Anthony J. Hanley, and Carol M. Anderson. Genetic variation in LMNA modulates plasma leptin and indices of obesity in aboriginal Canadians. Physiol Genomics 3: 39–44, 2000.—We previously showed that a rare mutation in LMNA, which encodes lamins A and C, underlies autosomal dominant Dunnigan-type familial partial lipodystrophy (FPLD). Because FPLD is an extreme example of genetically disturbed adipocyte differentiation, it is possible that common variation in LMNA is associated with obesity-related phenotypes. We therefore analyzed the relationships between the common LMNA 1908T/C single nucleotide polymorphism (SNP) and plasma leptin and anthropometric indices in 306 nondiabetic Canadian Oji-Cree. We found that subjects with the LMNA 1908T/1908T genotype had significantly higher plasma leptin than the subjects with either the 1908C/1908T or 1908C/1908C genotypes, after adjustment for age and sex. Physical indices of obesity, such as body mass index, percent body fat, and ratio of waist-to-hip circumference, were also higher among Oji-Cree subjects with the LMNA 1908T/1908T genotype than the subjects with either the 1908C/1908T or 1908C/1908C genotypes. The results suggest that common genetic variation in LMNA may be an important determinant of plasma leptin and obesity-related quantitative traits.

association study; complex disease; metabolism; obesity

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