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Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-γ2 (PPARγ-2) gene is associated with greater insulin sensitivity and decreased risk of type 2 diabetes in an Iranian population

  • Reza Meshkani , Mohammad Taghikhani , Bagher Larijani , Yadollah Bahrami , Shohreh Khatami , Ehteram Khoshbin , Amir Ghaemi , Sedigheh Sadeghi , Fatemeh Mirkhani , Azam Molapour and Khosrow Adeli
Published/Copyright: April 17, 2007
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Clinical Chemistry and Laboratory Medicine (CCLM)
From the journal Volume 45 Issue 4

Abstract

Background: The Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-γ2 (PPARγ-2) gene has been variably associated with insulin resistance, obesity and type 2 diabetes in several populations. However, this association has not been studied in Iranian subjects and we hypothesized that this variation might be associated with insulin resistance, type 2 diabetes and related metabolic traits in this population.

Methods: The Pro12Ala genotypes were determined by PCR-restriction fragment length polymorphism in 696 unrelated subjects including 412 non-diabetic controls and 284 type 2 diabetic patients.

Results: The frequency of the Ala allele was 9.4% and 5.9% in controls and type 2 diabetic subjects, respectively [adjusted odds ratio (OR) 0.457, p=0.005]. The Ala allele did not show a significant effect on anthropometric and biochemical parameters in the type 2 diabetic group, whereas in non-diabetic subjects, carriers of the Ala allele had significantly lower fasting insulin (p=0.007) and homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.009) levels compared to Pro/Pro subjects. Multivariate logistic regression analysis showed that Pro12Ala polymorphism was an independent determinant of type 2 diabetes in this population.

Conclusions: Our results for a sample of Iranian type 2 diabetes cases and controls provide evidence that the Pro/Ala genotype of the PPARγ-2 gene is associated with insulin sensitivity and may also have protective role against type 2 diabetes.

Clin Chem Lab Med 2007;45:477–82.


Corresponding author: Mohammad Taghikhani, c/o Reza Meshkani, Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modarres University, PO Box 14115-331, Tehran, Iran Phone: +98-21-88011001, Fax: +98-21-88013030,

Received: 2006-11-15
Accepted: 2007-1-13
Published Online: 2007-04-17
Published in Print: 2007-04-01

©2007 by Walter de Gruyter Berlin New York

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