The Role of Abdominal Obesity in the Pathogenesis of Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders that affects about 14-20% of women at reproductive ages and is associated with hyperandrogenism, hyperinsulinemia, ovarian disfunction and obesity especially abdominal obesity (AO). Due to its complex manifestations, the full pathogenic mechanism of PCOS is not fully understood. Here in, we provide an in-depth discussion about PCOS pathogenesis especially the role of AO in the progression of PCOS. In the present review article, the published studies in PubMed, Science Direct, Google Scholar gateway and databases were assessed using the keywords Polycystic ovary syndrome, Pathogenesis, abdominal obesity, insulin resistance, and hyperinsulinemia using the "and" and "or" operators from January 2017 to December 2021. The increasing prevalence of obesity in recent years has led to an increase in the prevalence of obesity-related diseases, including PCOS. Obesity, especially AO has important role in the pathogenesis of PCOS and its related complications including hyperinsulinemia, hyperandrogenism and insulin resistance (IR). It is estimated that AO observes in approximately 40- 80% of PCOS patients and is associated with IR, which counts as one of the main side effects of PCOS. It has been revealed that AO can significantly reduce the insulin sensitivity in normal weight PCOS patients with hyperandrogenism. In addition, IR, which is exacerbated by AO, can cause more accumulation of fat in the peritoneal region, creating a vicious feedback cycle between IR and obesity in patients with PCOS. Recent studies suggest that AO may play a more important role in the etiology of the PCOS than previously thought, Due to the underlying role of AO in causing and exacerbating other complications. It can improve the results of treatment ART cycles and be effective in controlling the complications caused by the PCOS. Keywords * Polycystic ovary syndrome * Obesity, abdominal * Insulin resistance * Hyperinsulinemia