Suppression of nutrient-induced inflammation with a nonsteroidal anti-inflammatory agent ameliorates ovarian dysfunction in lean insulin-sensitive women with polycystic ovary syndrome (PCOS)

Abstract

early follicular phase. TNFa, IL-27, IL-35, IL-37, a-1 acid glycoprotein were measured by a high sensitivity ELISA, while CRP, testosterone (T), androstenedione (AE), SHBG, DHEA-S levels were measured by RIA. Free androgen index (FAI) was calculated as percentage ratio of total testosterone to SHBG values. RESULTS: Levels of inflammatory mediators (CRP, TNFa, a-1 acid glycoprotein) were significantly increased in obese PCOS patients compared to obese controls and in lean PCOS patients compared to lean controls (all p<0.001). Levels of cytokines with anti-inflammatory properties (IL-27, IL-35, IL-37) were significantly decreased in obese PCOS patients compared to obese controls and in lean PCOS patients compared to lean controls (all p<0.001). Levels of T, androstenedione, DHEA-S were significantly increased, while level of SHBG was significantly increased in obese PCOS patients compared to obese controls and in lean PCOS patients compared to lean controls (all p<0.001). When obese and lean PCOS patients were compared, levels of IL-27, IL-35, IL-37 were significantly lower, while level of a-1 acid glycoprotein was significantly higher in obese PCOS patients compared lean patients (all p<0.001). FAI was higher in obese PCOS patients compared to obese controls, PCOS leans patients compared to lean controls (both p<0.001). BMI had a strong negative correlation with IL-27, IL-25, IL-37 and a positive correlation with a-1 acid glycoprotein (all p<0.001). FAI had a strong positive correlation with CRP, TNFa, a-1 acid glycoprotein and a negative correlation with IL-27, IL-25, IL-37 (all p<0.001). BMI had a positive correlation with FAI (p<0.05). CONCLUSIONS: The findings of the present study further confirm the pro-inflammatory state of PCOS.Moreover, obesity along with PCOS significantly elevates the inflammatory status and hyperandrogenism. Supported by: This research received funding from the Scientific Research Projects Coordination Unit of Istanbul University (grant 31834).