alexa Does Resistin Gene Polymorphisms +299 (G>A) Participate
ISSN: 2472-128X

Journal of Clinical & Medical Genomics
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Research Article

Does Resistin Gene Polymorphisms +299 (G>A) Participate in Insulin Resistance in Egyption Non-obese Type 2 Diabetes?

Osama Khalil1, Alsayed Alnahal1*, Mohamed Ghonium1, Samy Fawzy2, Magdy Ibrahem2, Nermin Raafat2 and Walaa Samy2

1Department of Internal Medicine, Zagazig University Hospital, Egypt

2Department of Medical biochemistry, Zagazig university Hospital, Egypt

*Corresponding Author:
Alsayed alnahal
Internal Medicine Department
Zagazig University Hospital, Egypt
Tel: 00201113174798
E-mail: [email protected]

Received Date: April 18, 2014; Accepted Date: June 25, 2014; Published Date: July 07, 2014

Citation: Khalil O, Alnahal A, Ghonium M, Fawzy S, Ibrahem M, et al. (2014) Does Resistin Gene Polymorphisms +299 (G>A) Participate in Insulin Resistance in Egyption non-Obese Type 2 Diabetes? Int J Genomic Med 2:117. doi: 10.4172/2332-0672.1000117

Copyright: © 2014 Khalil O, 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.



Background: Insulin Resistance (IR) is a condition which precedes the development of type 2 diabetes mellitus (T2DM). Resistin is a hormone secreted by adipocytes. Resistin gene (RETN) polymorphisms has been found to be associated with obesity and insulin resistance. We choose 60 patients have known type 2 diabetes mellitus against 45 healthy subjects to investigate the relationship between RETN +299 gene polymorphisms and insulin resistance, in non-obese patients with T2DM. Results: The present study revealed statistically significant increase in AA and combined GA+AA genotypes (with ODD Ratio 4.04 and 4.75 respectively), and statistically significant decrease in GG genotype in non-obese T2DM as compared to the control subjects. Also we found statistically significant increase in A allele and serum resistin in T2DM group as compared to the control group. In addition there were statistically significant increase in mean value ± SD of fasting blood glucose, insulin, HOMA-IR, HbA1C%, Resistin, total cholesterol, triglyceride, LDL-C and statistically significant decrease in mean value ± SD in serum HDL-C in AA combined AA+GA subgroups as compared to GG subgroup of T2DM group. Conclusions: Our study has shown that resistin +299G/A is  an important genetic regulator that resulted hyperresistinemia and subsequently  may be predisposing factor the development of T2DM in non-obese Egyptian population.


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