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Translational Biomedicine

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Abstrato

The Influence of Oxidative Stress in Inflammatory Process and Insulin Resistance in Obese Women with Polycystic Ovary Syndrome

Ana Celly Souza dos Santos, George Dantas Azevedo and Telma Maria Araújo Moura Lemos

Oxidative stress induced by reactive oxygen species (ROSs) may be associated with the development of inflammation and insulin resistance (IR) in obese women with polycystic ovary syndrome (PCOS).

Objectives: To evaluate the markers of oxidative stress, of inflammation, and of insulin resistance in obese women with PCOS and in healthy ovulatory women.

Methods: The parameters of oxidative stress, glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thiobarbituric acid reactive species (TBARSs), inflammatory markers such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) were evaluated in serum samples from 20 women in reproductive age. The volunteers were divided into two groups: Group I (obese control, n=10); Group II (PCOS obese, n=10). The categorization of groups was performed using body mass index (BMI), according to the World Health Organization (WHO) that classifies as obesity a BMI > 30 kg/m². Insulin resistance was also determined by the HOMA-IR index.

Results: The obese PCOS group compared to the equivalent BMI control group showed increased levels of GSH (387 mol/mol Hb ± 138 mol/mol Hb), CAT (366 k/gHb/min ± 20 k/gHb/min), TBARSs (7.2 MU/mol Hb ± 1 MU/mol Hb), CRP (2.35 mg/L ± 0.55 mg/L), basal insulin (16.88 μIU/mL ± 13.00 μIU/mL), with p=0.01, and HOMA-IR (2.16 ± 2.54 ) (p=0.04) associated with a decrease in antioxidant enzymes SOD (35 ± 12 MU/mol Hb) and GSH-Px (22 MU/molHb ± 11 MU/molHb) (p = 0.01). Correlations were also observed between the oxidative stress parameters of inflammation and of insulin resistance evaluated in women with PCOS.

Conclusion: The PCOS group had inflammation through elevated CRP and IR levels that can be aggravated with the production of ROSs, influencing the development of changes in glucose metabolism and of CVD related to the syndrome.