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The association of miR-27a (rs895819) polymorphism with the risk of type 2 diabetes
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| Soyar Sari , Ramak Badr |
| Department of Molecular and Cellular Sciences , Faculty of Advanced Sciences and Technology, Pharmaceutical Sciences Branch, Islamic Azad University, Tehran-Iran (IAUPS) , sari.s@iaups.ac.ir |
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Abstract: (1378 Views) |
Background and aims: Type 2 diabetes is an endocrine desease and one of the most common metabolic diseases in the world, and some environmental factors and genetic background are involved in the disease. Genetically, a large number of gene polymorphisms have been identified to be associated with this disease, but few studies have been conducted in polymorphisms miRNA and their correlation with type 2 diabetes. Among miRNAs, miR-27a involves in the predisposition to type 2 diabetes, and mutations can alter the miR-27a function and cause diabetes. The aim of the present study was to investigate the association of miR-27a (rs895819) with the risk of type 2 diabetes.
Methods: In the present case-control study, 100 type 2 diabetes patients and 100 healthy individuals were randomly selected. Polymorphism miR-27a (rs895819) was investigated using PCR-RFLP method. To determine the balance or imbalance in two groups and the relationship between polymorphisms and the incidence of type 2 diabetes, Chi-square test was applied.
Results: Significant differences in the genotype distribution of miR-27a (rs895819) in patients with type 2 diabetes in comparison to the healthy subjects indicated a P value equal to 0.038 (odds ratio: 2.63, 95% CI: 1.07-6.05).
Conclusion: The results suggested that there is an association between miR-27a genetic variants and the incidence of type 2 diabetes. However, further studies are needed to evaluate the significance of genetic variants in different populations.
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| Keywords: miR-27a, Polymorphism, Diabetes and DraIII restriction enzymes. |
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Full-Text [PDF 1033 kb]
(349 Downloads)
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Type of Study: Research |
Subject:
genetic
Received: 2016/07/6 | Accepted: 2017/01/8 | Published: 2017/08/2
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