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Title: Serum resistin and polymorphisms of androgen receptor CAG<inf>n</inf> and GGN<inf>n</inf> and aromatase TTTA<inf>n</inf>
Authors: González Hernández, A.
Cabrera De León, A.
Dominguez Coello, S.
Almeida González, D.
Rodríguez Pérez, M. C.
Brito Díaz, B.
Aguirre-Jaime, A.
Díaz-Chico, B. N. 
Keywords: Polycystic-Ovary-Syndrome
Repeat Polymorphism
Cyp19 Gene, et al
Issue Date: 2008
Journal: Obesity 
Abstract: There is evidence that androgens are regulators of insulin resistance (IR), and may be involved in the regulation of resistin, a cytokine that has been related with IR. Earlier studies found that androgen receptor length polymorphisms CAG(n) and GGN(n) and the aromatase polymorphism TTTA(n) may influence receptor or enzyme activity and serum concentrations of androgens. This study was designed to determine whether polymorphism length was related to serum resistin concentration and to other variables related with IR. In 1,580 persons chosen randomly from the general population of the Canary Islands (Spain), we measured polymorphism length, waist circumference, waist/hip ratio, BMI, and serum glucose concentration. In smaller subgroups, we also measured C-peptide (n = 677), resistin (n = 583), and leptin concentration (n = 754) and estimated IR (homeostasis model assessment-IR (HOMA2-IR)). In men, polymorphism length correlated with resistin concentration (CAG(n), r = 0.13, P = 0.031; TTTA(n), r = 0.15, P = 0.005; GGN(n), r = -0.15, P = 0.026), and the correlations were confirmed in multivariate regression models. The length of CAG(n) and TTTA(n) correlated inversely with C-peptide (r = -0.13, P = 0.016 and r = -0.21, P < 0.001, respectively) and with estimated IR (r = -0.12, P = 0.032 and r = -0.19, P 0.001, respectively). In men, length of the CAG(n), GGN(n), and TTTA(n) was associated with serum resistin concentration. These results support the hypothesis that androgens may be involved in the regulation of resistin. Resistin may be a link between IR and androgens.
ISSN: 1930-7381
DOI: 10.1038/oby.2008.289
Source: Obesity[ISSN 1930-7381],v. 16, p. 2107-2112
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