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Common Variation in LMNA Increases Susceptibility to Type 2 Diabetes and Associates With Elevated Fasting Glycemia and Estimates of Body Fat and Height in the General Population

Studies of 7,495 Danish Whites

¹ Steno Diabetes Center, Gentofte, Denmark
² Research Centre for Prevention and Health, Glostrup University Hospital, Glostrup, Denmark
³ Faculty of Health Science, University of Aarhus, Aarhus, Denmark

Address correspondence and reprint requests to Lise Wegner, MSc, Niels Steensens Vej 2, NSP1.03, DK-2820 Gentofte, Denmark. E-mail: lwgn{at}steno.dk

Abbreviations: IFG, impaired fasting glucose; IGT, impaired glucose tolerance; OGTT, oral glucose tolerance test; SNP, single nucleotide polymorphism

Mutations in LMNA encoding lamin A and C proteins cause monogenic syndromes characterized by muscular dystrophy and familial partial lipodystrophy. Eight tag single nucleotide polymorphisms in the LMNA locus were genotyped in 7,495 Danish whites and related to metabolic and anthropometric traits. The minor T-allele of rs4641 was nominally associated with type 2 diabetes (odds ratio 1.14 [95% CI 1.03–1.26], P = 0.01) in a study of 1,324 type 2 diabetic patients and 4,386 glucose-tolerant subjects and with elevated fasting plasma glucose levels in a population-based study of 5,395 middle-aged individuals (P = 0.008). The minor T-allele of rs955383 showed nominal association with obesity in a study of 5,693 treatment-naïve subjects (1.25 [1.07–1.64], P = 0.01), and after dichotomization of waist circumference, the minor alleles of rs955383 and rs11578696 were nominally associated with increased waist circumference (1.14 [1.04–1.23], P = 0.003; 1.12 [1.00–1.25], P = 0.04). The minor G-allele of rs577492 was associated with elevated fasting serum cholesterol and short stature (P = 3.0 · 10^–5 and P = 7.0 · 10^–4). The findings are not corrected for multiple comparisons and are by nature exploratory. However, if replicated, these findings suggest that less severe variation in a gene locus known to harbor severe mutations causing monogenic syndromes may modestly increase susceptibility to common metabolic and anthropometrical phenotypes of polygenic origin.

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