期刊
ARCHIVES OF MEDICAL RESEARCH
卷 47, 期 5, 页码 331-339出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.arcmed.2016.08.007
关键词
Obesity; Oxidative disturbance; Superoxide dismutase; Catalase; Genetic polymorphisms
资金
- Octava Convocatoria Para Financiamiento de Proyectos de Investigacion through the Research Direction of Universidad Iberoamericana Ciudad de Mexico
Background and Aims. Oxidative disturbance is an important factor involved in the etiology of comorbidities associated with obesity. Genetic polymorphisms such as SOD1 -251A > G, SOD2 47 C > T, CAT -21A > T and CAT -262 C> T have been described to alter the activity of antioxidant enzymes. The aim of the present work was to analyze the association of the mentioned SNPs with obesity and their relationship with anthropometric and clinical variables in this group. Methods. The study included 416 Mexican women (208 normal weight, NW and 208 subjects with obesity, OB). Dietary intake, anthropometric, biochemical and clinical features were evaluated and then analyzed in function of the genotypes. Results. The mutated carriers (GA+GG) of SOD -251 were significantly higher in the OB group (0.24) compared to the NW group (0.08). The other SNPs showed no differences compared with control group. When comparing carrier mutated subjects with obesity vs. wild-type obese participants with the SNPs SOD1 -251, SOD2 47 and CAT -262, the carriers showed a significantly (p < 0.05) higher value in body fat percentage. Also, carriers of SOD2 47 and CAT -262 showed significantly higher values (p = 0.002) and (p = 0.01), respectively, when visceral fat was compared between groups. Systolic blood pressure was significantly higher (p = 0.02) in carriers of mutated CAT-21. Conclusion. SOD1 -251A > G is associated with obesity independent of the presence of diabetes or dyslipidemia. Mutated obese carries of SOD1 -251, SOD2 47 and CAT -262 are associated with a higher distribution of fat in comparison with obese wild-type carriers. (C) 2016 IMSS. Published by Elsevier Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据