Эндокринология и метаболический синдром
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ISSN: 2161-1017
ISSN: 2161-1017
Pablo A. Montiel-Tellez BS, Adriana Nieva-Vazquez, Leonardo M. Porchia, Elba Gonzalez-Mejia M, Enrique Torres-Rasgado, Guadalupe Ruiz-Vivanco and Ricardo Perez-Fuentes
Objective: To determine the association between the c.+62G>A and g.-420C>G polymorphisms and Type 2 Diabetes (T2D) or obesity susceptibility for Mexicans. Additionally, we examined their overall effect across different populations by a systematic review.
Methods: 164 Mexicans were classified as Healthy, Obese, or T2D. Genotypes were determined and associated risk for the heterozygous, homozygous, dominant, recessive, and allelic genetic models were determined by calculating the Odds Ratios (OR). For the meta-analysis, original publications that had determined RETN polymorphisms in T2D or obese subjects were searched for in PubMed, Scopus, EBSCO, Ovid, and Wiley databases until November 2015, using the search terms: T2D, obesity, RETN, and polymorphism. Pooled ORs were computed using a random-effects or fixed-effects models.
Results: For our cohort, no associations were observed between the polymorphisms and obesity or T2D. The metaanalysis indicates an increased risk of obesity among carriers of the g.-420G allele for the heterozygous and dominant models (OR=1.33 and OR=1.30, p<0.05, respectively). By regional assessment, Africans were associated with an elevated risk of developing T2D (OR=2.35-7.17, p<0.05) and obesity (OR=1.54-2.13, p<0.05). North Americans had an increased risk of developing obesity for the heterozygous and dominant models (OR=1.49and OR=1.42, p<0.05, respectively). No associations were determined between the c.+62 polymorphism and obesity or T2D.
Conclusion: For Mexicans, none of the polymorphisms were associated with a risk of developing obesity or T2D. However, there is an increased risk of developing obesity for the whole population for subjects who carry the g.-420G allele.