Abstract
The association between some Tumor necrosis factor-alpha (TNF-α) promoter polymorphisms and Type 2 diabetes mellitus (T2DM) remains controversial. Ethnic differences may play a role in these conflicting results. The aim of this study was to investigate the association between −308G/A and −238G/A polymorphisms located in the promoter region of the TNF-αgene and T2DM in Mexican mestizo patients. Nine hundred four individuals (259 patients with T2DM and 645 controls) were genotyped for the −308G/A and −238G/A polymorphisms by PCR—RFLP. We found that the −238A allele increased the risk of developing T2DM in Mexican patients (OR = 1.57, 95% CI: 1.07–2.29;p= 0.018). Moreover, we found that the frequency of the GA haplotype (created by the −308G and −238A alleles) was significantly increased in patients with T2DM when compared with controls (OR = 1.56, 95% CI: 1.05–2.31;p= 0.026). Our results suggest that the −238G/A polymorphism and a specific haplotype (GA) are genetic risk factors for the development of T2DM in Mexican population.
Highlights
Type 2 diabetes mellitus is a major worldwide public health problem
Because it has been suggested that the −308G/A and −238G/A polymorphisms are associated with insulin resistance, obesity, and Type 2 diabetes mellitus (T2DM) in different ethnic groups [9,10], the purpose of this study was to examine the association between these polymorphisms and T2DM in Mexican diabetic subjects
Odds ratio shows that individuals bearing the A/A genotype have a risk of 6.92 for developing T2DM assuming a co-dominant model (G/G vs. AA)
Summary
Type 2 diabetes mellitus is a major worldwide public health problem. The International Diabetes Federation estimates that 285 million people have the disease in 2010, which represents 6.4% of the global adult pop-ulation [1]. Type 2 diabetes mellitus is a major worldwide public health problem. The International Diabetes Federation estimates that 285 million people have the disease in 2010, which represents 6.4% of the global adult pop-. It has been suggested that inflammatory cytokines impair insulin signalling; genes that regulate cytokine responses are candidate genes for association with insulin resistance and T2DM [2, 3]. It was established that TNF-α is mainly synthesized and secreted from macrophages infiltrated in the adipose tissue and plays a key role in the pathogenesis of obesity and in the insulin-resistant state [5,6]. TNF-α can cause insulin resistance in vitro and in vivo and may affect carbohydrate metabolism by decreasing both insulin-stimulated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
