Endocrinology Research and Practice
Original Article

Association Between Pro12Ala Polymorphism of Peroxisome ProliferatorActivated Receptor Gamma (PPARγ) and Components of Metabolic Syndrome


Hacettepe University, School of Medicine, Departtment of Endocrinology and Metabolism, Ankara, Turkey

Endocrinol Res Pract 2010; 14: 54-59
Read: 720 Downloads: 217 Published: 01 September 2010

 Metabolic syndrome is a highly prevalent complex disorder characterized by abdominal obesity, insulin resistance, dyslipidemia and hypertension. It occurs as a result of the interaction between genetic susceptibility and environmental factors, in particular, diet. The pro12Ala polymorphism of peroxisome proliferator-activated receptor gamma (PPARg), which generates a genetic diversity has been proposed to act in the pathogenesis of metabolic syndrome. The objectives of this study were to verify whether PPARg Pro12Ala polymorphism modulates the prevalence of the components of metabolic syndrome and whether dietary intake interacts with the polymorphism to modulate the features of syndrome.
Materials and Methods: A total of 150 subjects (aged 18-65) diagnosed as having metabolic syndrome according to the International Diabetes Federation (IDF) criteria participated in the study. All subjects underwent a clinical, anthropometrical, biochemical and nutritional assessment and analysis of Pro12Ala polymorphism of PPARg at the Department of Nutrition and Dietetics and Department of Endocrinology - Metabolism, Hacettepe University.
Results: The polymorphism was detected in 14% of the study population (1.3% - AlaAla homozygote and 12.7% - AlaPro heterozygote). The prevalence of any of the syndrome components defined by IDF did not differ significantly with PPARg genotype. In addition, no association was found between dietary intake and prevalence of metabolic syndrome components modified by PPARg Pro12Ala genotype.
Conclusion: Our results suggest that PPARg Pro12Ala polymorphism is not associated with the metabolic syndrome components and cannot modulate the association between dietary intake and components of the metabolic syndrome. 


EISSN 2822-6135