Association of Interleukin-10 (-592A/C) Gene Polymorphism with its Level in Type 2 Diabetes Mellitus with and without Nephropathy
- Corresponding Author:
- Aida A. Mahmoud
Medical Biochemistry, Sohag University, Egypt
E-mail: [email protected]
Received date: November 23, 2015 Accepted date: January 20, 2016 Published date: January 25, 2016
Citation: Mahmoud AA, Sheneef A, Sayed AA, Ezat MAW, Sabet EA (2016) Association of Interleukin-10 (−592A/C) Gene Polymorphism with its Level in Type 2 Diabetes Mellitus with and without Nephropathy. J Mol Genet Med 10:199. doi:10.4172/1747-0862.1000199
Copyright: © 2016 Mahmoud AA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objectives: Several candidate genes are implicated in the pathogenesis of type 2 diabetes mellitus (T2DM), one of which is interleukin (IL-10). In this investigation, we aimed to study the association between IL-10 (-592A/C) gene polymorphism with its level in T2DM with and without nephropathy.
Methods: IL-10 (-592A/C) gene polymorphism was genotyped using restriction fragment length polymorphism (RFLP-PCR) technique and IL-10 levels were measured in two groups of T2DM, one group complicated with nephropathy and the second non-complicated.
Results: Our results revealed no significant differences in IL-10 (−592A/C) genotypes distribution between the two groups of T2DM patients. IL-10 levels were found significantly elevated in diabetic nephropathy patients compared to T2DM without nephropathy (P<0.05) and were positively correlated to the degree of albuminuria (r=0.61, P<0.01). IL-10 levels increased in IL-10- (−592C/C) genotype compared to IL-10-(−592A/A) and IL-10- (−592A/C) genotypes in diabetic nephropathy patients while such difference was not found in T2DM patients without nephropathy.
Conclusion: IL-10 (-592A/C) gene polymorphism and IL-10 level play a role in the pathogenesis of nephropathy in T2DM.