Abstract:
: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.
journal_name
Diabetesjournal_title
Diabetesauthors
Dahlman I,Kaaman M,Jiao H,Kere J,Laakso M,Arner Pdoi
10.2337/diabetes.54.10.3032subject
Has Abstractpub_date
2005-10-01 00:00:00pages
3032-4issue
10eissn
0012-1797issn
1939-327Xpii
54/10/3032journal_volume
54pub_type
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