High concentration of chemerin caused by ovarian hyperandrogenism may lead to poor IVF outcome in polycystic ovary syndrome: a pilot study.

A chronic low-grade inflammation state accounts for an important part of the pathogenesis of polycystic ovary syndrome (PCOS). The adipose tissue derived cytokine chemerin has recently been proven to be a proinflammatory chemokine, but its mechanism involved in the pathogenesis of PCOS remains largely unresolved. From non-obese patients with and without PCOS, follicular fluid and granulosa cells were retrieved. The effect of testosterone on the expression of chemerin and its receptors was explored in granulosa cells. IVF outcomes in different groups based on FF-chemerin (chemerin in the follicular fluid) level were further compared. The concentration of FF-chemerin, and the mRNA expression of chemerin and its receptors in granulosa cells from PCOS were significantly higher than those from non-PCOS. FF-chemerin was positively correlative to total testosterone (TT) and luteinizing hormone (LH) in the follicular fluid. Furthermore, testosterone upregulated the expression of chemerin and its receptors in vitro. The oocyte utilization rate and high-quality embryo rate were significantly decreased in the high FF-chemerin group. The upregulated chemerin levels in the ovary of PCOS patients, which may be caused by ovarian hyperandrogenism, may be a risk factor for oocyte maturation and embryo development. These findings may provide a basis for novel interventions to improve IVF outcomes.

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