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Diabetes 54:3032-3034, 2005
© 2005 by the American Diabetes Association, Inc.

Brief Genetics Reports

The CIDEA Gene V115F Polymorphism Is Associated With Obesity in Swedish Subjects

Ingrid Dahlman1, Maria Kaaman1, Hong Jiao2, Juha Kere2, Markku Laakso3, and Peter Arner1

1 Department of Medicine, Huddinge, Karolinska Institute, Stockholm, Sweden
2 Department of Biosciences, Clinical Research Center, Karolinska Institute, Stockholm, Sweden
3 Department of Medicine, Kuopio University Hospital, Kuopio, Finland

The cell death–inducing DFFA (DNA fragmentation factor-{alpha})-like effector A (CIDEA) gene is implicated as an important regulator of body weight in mice and humans and is therefore a candidate gene for human obesity. Here, we characterize common CIDEA gene polymorphisms and investigate them for association with obesity in two independent Swedish samples; the first comprised 981 women and the second 582 men. Both samples display a large variation in BMI. The only detected coding polymorphism encodes an exon 4 V115F amino acid substitution, which is associated with BMI in both sexes (P = 0.021 for women, P = 0.023 for men, and P = 0.0015 for joint analysis). These results support a role for CIDEA alleles in human obesity. CIDEA-deficient mice display higher metabolic rate, and the gene cross-talks with tumor necrosis factor-{alpha} (TNF-{alpha}) in fat cells. We hypothesize that CIDEA alleles regulate human obesity through impact on basal metabolic rate and adipocyte TNF-{alpha} signaling.

Address correspondence and reprint requests to Peter Arner, Professor, MD, Department of Medicine, Karolinska University Hospital, Huddinge, SE-141 86 Stockholm, Sweden. E-mail: peter.arner{at}medhs.ki.se

Abbreviations: CIDEA, cell death–inducing DFFA (DNA fragmentation factor-{alpha})-like effector A; SNP, single nucleotide polymorphism; TNF-{alpha}, tumor necrosis factor-{alpha}


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