Interplay of adipocytokines with polycystic ovary syndrome

The bioactive chemicals generated by adipose tissue control glucose and lipid metabolism and energy and immune system function. Inflammation of adipose tissue triggers signaling pathways known to alter metabolic homeostasis. Furthermore, dysregulation of bioactive chemicals leads to metabolic irregularities and long-term effects, particularly in obese people. Adipokines can be pro- or anti-inflammatory. Obesity is associated with an increase in proinflammatory adipokines and a decrease in anti-inflammatory adipokines. Globally, research has demonstrated that adipokines play a role in the etiology of disorders that impact practically all body systems. Polycystic ovary syndrome (PCOS) is the most common endocrine-metabolic disease in females of reproductive age. PCOS patients are more likely to develop metabolic issues such as type 2 diabetes mellitus (T2DM), insulin resistance (IR), and adipose tissue dysfunction. Numerous studies have found that obese PCOS patients have frequent adipose tissue malfunction and, as a result, changed adipokine levels, indicating that adipokines play a role in PCOS patients. The particular process through which adipokines contribute to the development of PCOS, however, remains uncertain. Vaspin, chemerin, resistin, leptin, omentin, adiponectin, apelin, asprosin, and visfatin have all been associated with PCOS. Exploring the interplay of novel adipokines with PCOS may aid clinicians in better diagnosing and managing PCOS and its complications. The current review would incorporate existing research on the relationship between adipokines with PCOS.