The CIDEA Gene V115F Polymorphism Is Associated With Obesity in Swedish Subjects
- 1Department of Medicine, Huddinge, Karolinska Institute, Stockholm, Sweden
- 2Department of Biosciences, Clinical Research Center, Karolinska Institute, Stockholm, Sweden
- 3Department of Medicine, Kuopio University Hospital, Kuopio, Finland
- 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
Abstract
The cell death–inducing DFFA (DNA fragmentation factor-α)-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-α (TNF-α) in fat cells. We hypothesize that CIDEA alleles regulate human obesity through impact on basal metabolic rate and adipocyte TNF-α signaling.
- CIDEA, cell death–inducing DFFA (DNA fragmentation factor-α)-like effector A
- SNP, single nucleotide polymorphism
- TNF-α, tumor necrosis factor-α
Footnotes
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- Accepted June 27, 2005.
- Received March 29, 2005.
- DIABETES
