Endocrine Abstracts (2011) 26 P103

Effect of paraoxonase genes on metabolic profile of women with polycystic ovary syndrome

N Xita, L Lazaros, I Georgiou & A Tsatsoulis


University of Ioannina, Ioannina, Greece.


Introduction: Increased oxidative stress is considered to be implicated in the pathophysiology of polycystic ovary syndrome (PCOS). While the regulation of oxidative stress is multifactorial, many studies have been focused on the antioxidant role of paraoxonase (PON). The aim of this study was to investigate the possible association of the Q192R and the L55M polymorphisms of PON1 and the Ser311Cys polymorphism of PON2 with PCOS.

Subjects and methods: We studied 165 women with PCOS and 168 healthy women. The body mass index (BMI) was recorded. Insulin resistance was assessed by fasting glucose to insulin ratio and HOMA index. Furthermore, 100 overweigh-obese patients underwent a 75gr OGTT and areas under the curve (AUC) for insulin and glucose were estimated. DNA was extracted from peripheral blood leucocytes and the Q192R and the L55M polymorphisms of PON1 and the Ser311Cys polymorphism of PON2 were genotyped.

Results: PON1 and PON2 gene polymorphisms were in Hardy–Weinberg equilibrium (P>0.05) in both PCOS and control group. There was no significant difference in the distribution of all polymorphisms between PCOS women and controls. However, the L55M polymorphism was found to be associated with insulin levels after glucose load. Patients with the LL genotype compared with those with LM or MM genotype, had higher AUCinsulin values whereas the basal insulin concentrations, fasting glucose to insulin ratio, HOMA index and AUCglucose were similar. This association remained significant after adjustment for the confounding factors BMI, age, and AUCglucose (P=0.012, β=−0.243). Regarding the Q192R polymorphism of PON1 and the Ser311 polymorphism of PON2 no association with biochemical parameters was found.

Conclusion: PON1 and PON2 gene polymorphisms are not associated with PCOS. However, the association found between the L55M polymorphism and insulin levels after glucose load shows that this polymorphism may be implicated in the insulin resistant phenotype of PCOS.

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