Association of RETN +299(G>A) polymorphism with type two diabetes mellitus

Ghaith  Altawallbeh; Omar F. Khabour; Mahmoud A. Alfaqih; Muayad M. Abboud; Mohammad  Gharibeh; Najeeb A. Mohammed

doi:10.18388/abp.2020_5409

Ghaith Altawallbeh Department of Laboratory Medicine and Pathology, University of Minnesota, Minnesota, USA
Omar F. Khabour Department of Medical Laboratory Sciences, Jordan University of Science and Technology, Irbid, Jordan https://orcid.org/0000-0002-3006-3104
Mahmoud A. Alfaqih Department of Physiology and Biochemistry, Jordan University of Science and Technology, Irbid, Jordan
Muayad M. Abboud Department of Basic Medical Sciences, Hashemite University, Jordan
Mohammad Gharibeh Department of Laboratory Medicine and Pathology, University of Minnesota, Minnesota, USA
Najeeb A. Mohammed Department of Medical Laboratory Sciences, Jordan University of Science and Technology, Irbid, Jordan

DOI: https://doi.org/10.18388/abp.2020_5409

Abstract

The global prevalence of type-two diabetes mellitus (T2DM) makes it a disease of public health concern. T2DM is strongly linked with insulin resistance caused by increased levels of visceral fat. Visceral fat secretes several adipocytokines that regulate body metabolism. Resistin is one of these adipocytokines which is encoded by the RETN gene. Herein, we tested the association of the RETN +299(G>A) and −420(C>G) single nucleotide polymorphisms (SNPs) with T2DM. T2DM patients (n=282) and healthy subjects (n=125) were included in the study. Subjects with metabolic syndromes other than diabetes were excluded. Genotyping of subjects was performed using PCR-RFLP. The +299(G>A) SNP was associated with T2DM (P=0.038). The AA genotype was higher in T2DM (17%) compared to controls (8%) with an odd ratio of 2.16 and 95% CI of 1.34 to 4.56. With respect to −420(C>G) SNP, no significant association was found with the risk of T2DM (P=0.128). The haplotype analysis of the examined SNPs indicated that the CA haplotype of the −420 and +299 SNPs in RETN was associated with T2DM risk (P=0.004; odd ration 4.0, 95% CI: 1.56–10.0). In conclusion, the present findings suggest a role of the RETN locus in modulating the risk of T2DM.