Polycystic ovary syndrome: a multisystemic approach to metabolic dysfunctions – review

Polycystic ovary syndrome (PCOS) is a complex and mul­ti­fac­to­rial endocrine disorder predominantly af­fec­ting pre­me­no­pausal women, characterized by hyper­an­dro­ge­nism, chro­nic anovulation, and polycystic ovarian mor­pho­lo­gy. Hyper­androgenism, a central pathogenic factor, ne­ga­tively influences metabolism through its effects on va­rious tissues and organs, including adipose tissue, skeletal mus­cle, and the liver. The redistribution of adiposity towards visceral and intraperitoneal fat depots, driven by androgens, is cor­re­la­ted with an increased risk of abdominal obesity and in­su­lin resistance. In skeletal muscles, hyperandrogenism in­duces a decrease in insulin sensitivity by disrupting insulin sig­na­ling and mitochondrial function, thereby contributing to the metabolic dysfunctions associated with PCOS. At the hepatic level, women with PCOS exhibit a higher pre­va­lence of metabolic dysfunction-associated steatotic li­ver disease (MASLD), a relationship largely mediated by chro­nic inflammation and the proinflammatory effects of an­dro­gens. These findings underscore the importance of un­der­stan­ding the molecular mechanisms underlying the re­la­tion­ship between hyperandrogenism and metabolic dys­func­tions in PCOS, with significant implications for the de­ve­lop­ment of innovative and personalized therapeutic stra­te­gies. Given the high prevalence and significant impact of PCOS on metabolic health, future research should focus on elucidating these mechanisms and identifying more ef­fec­tive therapeutic approaches.