Wnt10a missense gene polymorphism association with obesity risk: List of literature and a case-control study with Roc analysis for serum β-catenin level in Egypt

Abstract

BackgroundGenome-wide association studies have been implicated in the pathogenesis of several diseases including obesity. Few Recent studies reported wnt10a protein as a negative regulator for the adipogenesis process. However, to our knowledge, no studies discussed the role of SNP in the mechanism through which wnt10a gene mediate its role in adipogenesis suppression. Objectiveswe intended to investigate the association between missense and non-sense pathogenic polymorphisms of wnt10a gene and obesity risk in the Egyptian population. In addition, we aimed to determine the diagnostic accuracy of serum β-catenin level, an important modulator of Wnt/β-catenin signaling in the obesity pathogenesis. It is worth noting, that it is the first study to discuss wnt10a gene polymorphisms and serum β-catenin level with obesity risk. MethodsOur study included 96 obese and 102 non-obese of unrelated Egyptian volunteers. All the subjects underwent measurement the level of serum fasting glucose level, lipid profile, serum β-catenin, and CBC. RFLP-PCR method was used to genotype both wnt10a gene polymorphisms (rs121908119-rs141074983). ResultsOur results showed that missense polymorphism of arginine to cysteine (rs141074983) SNP may be associated with obesity risk under different genetic models. The minor allele carrier (CT and TT) was highly associated with obesity (OR = 3.7 (1.3–7.07), p = 0.006). In contrast, the decrease in serum β-catenin level in obese than non-obese volunteers lacked the required statistical confidence (p > 0.05). ConclusionThe substitution of arginine to cysteine (rs141074983) in wnt10a gene is strongly associated with increased risk for obesity in the Egyptian population and larger studies can confirm our results.