Association of polymorphisms at the ADIPOR1 regulatory region with type 2 diabetes and body mass index in a Brazilian population with European or African ancestry

Author(s)

Yeh, E. ^[1] ; Kimura, L. ^[1] ; Errera, F. I. V. ^{[1, 2]} ; Angeli, C. B. ^[1] ; Mingroni-Netto, R. C. ^[1] ; Silva, M. E. R. ^[3] ; Canani, L. H. S. ^[4] ; Passos-Bueno, M. R. ^[1]

Affiliation

^[1] Univ Sao Paulo, Dept Genet & Biol Evolut, Inst Biociencias, Ctr Estudos Genoma Humano, BR-05508900 Sao Paulo - Brazil

^[2] Escola Super Ciencias, Dept Morfol, Vitoria, ES - Brazil

^[3] Univ Sao Paulo, Fac Med, Lab Invest Med LIM 18, Hosp Clin, Sao Paulo - Brazil

^[4] Univ Fed Rio Grande do Sul, Div Endocrinol, Hosp Clin Porto Alegre, Porto Alegre, RS - Brazil

• Document type: Journal article
• Source: Brazilian Journal of Medical and Biological Research; v. 41, n. 6, p. 468-472, JUN 2008.
• Web of Science Citations: 3

Abstract

Association studies between ADIPOR1 genetic variants and predisposition to type 2 diabetes (DM2) have provided contradictory results. We determined if two single nucleotide polymorphisms (SNP c.-8503G>A and SNP c.10225C>G) in regulatory regions of ADIPOR1 in 567 Brazilian individuals of European (EA; N = 443) or African (AfA; N = 124) ancestry from rural (quilombo remnants; N = 439) and urban (N = 567) areas. We detected a significant effect of ethnicity on the distribution of the allelic frequencies of both SNPs in these populations (EA: -8503A = 0.27; AfA: -8503A = 0.16; P = 0.001 and EA: 10225G = 0.35; AfA: 10225G = 0.51; P < 0.001). Neither of the polymorphisms were associated with DM2 in the case-control study in EA (SNP c.-8503G>A: DM2 group -8503A = 0.26; control group -8503A = 0.30; P = 0.14/SNP 10225C>G: DM2 group 10225G = 0.37; control group 10225G = 0.32; P = 0.40) and AfA populations (SNP c.-8503G>A: DM2 group -8503A = 0.16; control group -8503A = 0.15; P = 0.34/SNP 10225C>G: DM2 group 10225G = 0.51; control group 10225G = 0.52; P = 0.50). Similarly, none of the polymorphisms were associated with metabolic/anthropometric risk factors for DM2 in any of the three populations, except for HDL cholesterol, which was significantly higher in AfA heterozygotes (GC = 53.75 ± 17.26 mg/dL) than in homozygotes. We conclude that ADIPOR1 polymorphisms are unlikely to be major risk factors for DM2 or for metabolic/anthropometric measurements that represent risk factors for DM2 in populations of European and African ancestries. (AU)

• FAPESP's process: 98/14254-2 - The Human Genome Research Center
• Grantee: Mayana Zatz
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC