Pathophysiologic mechanisms of obesity- and chronic inflammation-related genes in etiology of polycystic ovary syndrome

One of the common heterogeneous reproductive disorders in women of childbearing age is polycystic ovary syndrome (PCOS). It is characterized by lack of fertility due to anovulatory cycles, hyperandrogenemia, polycystic ovaries, hyperinsulinemia, and obesity. Both reproductive anomalies and metabolic disorders are involved in PCOS pathology. Although the role of increased levels of androgens in initiation of PCOS is almost proven, mechanisms of PCOS pathophysiology are not clear. Here we discuss roles of altered metabolic conditions, obesity, and chronic inflammation in PCOS pathophysiology.

In this review, we attempted to identify genes related to obesity and chronic inflammation aspects of PCOS and their physiological functions to explain the pathways that are regulated by these genes and can be a prominent function in PCOS predisposition. For this purpose, published articles and reviews dealing with genetic evaluation of PCOS in women in peer-reviewed journals in PubMed and Google Scholar databases were included in this review.

Obesity and chronic inflammation are not prominent diagnostic features of PCOS, but they play an important role in exacerbating metabolic and hyperandrogenic states. ADIPOQ, FTO TGFβ, and DENND1A as the main obesity- and chronic inflammation-related genes have roles in PCOS pathophysiology.

It seems that genes related to obesity pathology in genomic research association, are related to metabolic aspects and body mass index in PCOS patients. Genomes have roles in chronic inflammation, followed by obesity, in the pathogenesis of PCOS.