Volume 6, Issue 2 (Int J Mol Cell Med 2017)                   Int J Mol Cell Med 2017, 6(2): 121-130 | Back to browse issues page


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Raza S T, Abbas S, Siddiqi Z, Mahdi F. Association between ACE (rs4646994), FABP2 (rs1799883), MTHFR (rs1801133), FTO (rs9939609) Gene Polymorphism and Type 2 Diabetes with Dyslipidemia. Int J Mol Cell Med 2017; 6 (2) :121-130
URL: http://ijmcmed.org/article-1-658-en.html
1- Department of Biochemistry, Era’s Lucknow Medical College and Hospital, Lucknow, India. , tasleem24@gmail.com
2- Department of Biochemistry, Era’s Lucknow Medical College and Hospital, Lucknow, India.
3- Department of Medicine Era’s Lucknow Medical College and Hospital, Lucknow, India.
Abstract:   (9115 Views)

Diabetic dyslipidemia is one of the leading causes of coronary artery disease (CAD) death. Genetic and environmental factors play an important role in the development of type 2 diabetes mellitus (T2DM) and dyslipidemia. The present study was aimed to investigate the association of ACE (rs4646994), FABP2 (rs1799883), MTHFR (rs1801133) and FTO (rs9939609) genetic polymorphism in T2DM with dyslipidemia. Totally, 559 subjects including 221 T2DM cases with dyslipidemia, 158 T2DM without dyslipidemia and 180 controls were enrolled. ACE genetic polymorphism was evaluated by polymerase chain reaction (PCR), while MTHFR, FABP2, ​FTO genetic polymorphisms were evaluated by PCR and restriction fragment length polymorphism (RFLP). Significant association of ACE and MTHFR genetic polymorphisms were found in both group of cases [T2DM with dyslipidemia (P<0.001, and P=0.008, respectively) and T2DM without dyslipidemia (P=0.003, and P=0.010, respectively)] while FABP2 and FTO genetic polymorphisms were significantly associated with T2DM without dyslipidemia (P=0.038, and P= 0.019, respectively). This study concludes that ACE, FABP2, FTO and MTHFR genes are associated with T2DM. Additionally, it also seems that ACE and MTHFR genes might be further associated with the development of dyslipidemia in T2DM cases.

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Type of Study: Original Article | Subject: Genetics & Disease
Received: 2017/02/17 | Accepted: 2017/06/3 | Published: 2017/06/24

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