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Purpose: Fractalkine (FKN) is an inflammatory chemokine related to reproductive system and glucose metabolism. There is a link between FKN and steroidogenesis as FKN induces progesterone synthesis. Polycystic ovary syndrome (PCOS) is a common reproductive and metabolic disorder associated with low progesterone production and insulin resistance. We aimed to explore whether women with PCOS have any difference in FKN levels compared to women without PCOS. We also focused on determination of any association between FKN levels and hormonal-metabolic parameters in women with PCOS., Methods: The current research was designed as a case-control study. Eighty subjects with PCOS and 80 age- and body mass index (BMI)-matched subjects with normal menstrual cycle were taken into the study. We measured circulating FKN levels via ELISA methods., Results: Circulating FKN levels were higher in women with PCOS than controls (1.93 ± 0.61 vs. 1.22 ± 0.33 ng/ml, P< 0.001). FKN levels showed a positive correlation with body mass index (BMI), insulin resistance, inflammatory marker hs-CRP, total testosterone, and free-androgen index (FAI), whereas it showed a negative correlation with sex hormone-binding protein in women with PCOS. Linear regression analyses revealed that the link of FKN with BMI, insulin resistance, hs-CRP, and FAI was independent. Binary logistic regression analysis showed that the risk of having PCOS was associated with high levels of FKN., Conclusions: Increased FKN levels related to insulin resistance, inflammation and androgens in women with PCOS. FKN may have an inter-related role in different pathophysiologic pathways of PCOS.

Betatrophin is a newly identified hormone determined to be a potent inducer of pancreatic beta cell proliferation in response to insulin resistance in mice. Polycystic ovary syndrome (PCOS) is an inflammatory-based metabolic disease associated with insulin resistance. However, no evidence is available indicating whether betatrophin is involved in women with PCOS. The objective of this study was to ascertain whether betatrophin levels are altered in women with PCOS. This study was conducted in secondary referral center. This cross-sectional study included 164 women with PCOS and 164 age- and BMI-matched female controls. Circulating betatrophin levels were measured using ELISA. Metabolic and hormonal parameters were also determined. Circulating betatrophin levels were significantly elevated in women with PCOS compared with controls (367.09 ± 55.78 vs. 295.65 ± 48.97 pg/ml, P < 0.001). Betatrophin levels were positively correlated with insulin resistance marker homeostasis model assessment of insulin resistance (HOMA-IR), free-testosterone, high-sensitivity C-reactive protein (hs-CRP), atherogenic lipid profiles, and BMI in PCOS. Multivariate logistic regression analyses revealed that the odds ratio for PCOS was 2.51 for patients in the highest quartile of betatrophin compared with those in the lowest quartile (95 % CI 1.31-4.81, P = 0.006). Multivariate regression analyses showed that HOMA-IR, hs-CRP, and free-testosterone were independent factors influencing serum betatrophin levels. Betatrophin levels were increased in women with PCOS and were associated with insulin resistance, hs-CRP, and free-testosterone in these patients. Elevated betatrophin levels were found to increase the odds of having PCOS. Further research is needed to elucidate the physiologic and pathologic significance of our findings.

This study was designed to show the effect of propylthiouracil treatment on sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels on subjects with subclinical hyperthyroidism. After checking sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels of 35 patients with subclinical hyperthyroidism, each was given 50 mg tablets of propylthiouracil three times daily. After 3 months, sCD40L, high-sensitivity C-reactive protein, and fetuin-A levels were then compared to the levels before treatment. Although high-sensitivity C-reactive protein and sCD40L levels were normal in the subclinical hyperthyroidism patients compared to the healthy controls, fetuin-A levels were statistically significantly higher (*p = 0.022). After treatment, fetuin-A levels of subclinical hyperthyroidism patients decreased statistically significantly compared to the levels before treatment (**p = 0.026). sCD40L and high-sensitivity C-reactive protein levels did not have a statistically significant difference compared to the control group and post-propylthiouracil treatment. In subclinical hyperthyroidism patients, high fetuin-A levels before propylthiouracil treatment and decreases in these levels after treatment in cases with subclinical hyperthyroidism indicated the possibility of preventing long-term cardiac complications with propylthiouracil treatment.