Rodent models in polycystic ovarian syndrome: Dissecting reproductive and metabolic phenotypes for therapeutic advancements

Abstract

The most prevalent reason for female infertility is polycystic ovarian syndrome (PCOS) exhibiting two of three phenotypes including biochemical or clinical hyperandrogenism, anovulation and polycystic ovaries. Insulin resistance and obesity are common in PCOS-afflicted women. Androgens are thought to be the primary cause of PCOS causing symptoms including anovulation, follicles that resemble cysts, higher levels of the luteinizing hormone (LH), increased adiposity, and insulin resistance. However, due to the heterogeneity of PCOS, it is challenging to establish a single model that accurately mimics all the reproductive and metabolic phenotypes seen in PCOS patients. In this review, we aimed to investigate rodent models of PCOS and related phenotypes with or without direct hormonal treatments and to determine the underlying mechanisms to comprehend PCOS better. We summarized rodent models of PCOS that includes direct and indirect hormone intervention and discussed the aetiology of PCOS and related phenotypes produced in rodent models. We presented combined insights on multiple rodent models of PCOS and compared their reproductive and/or metabolic phenotypes. Our review indicates that there are various models for studying PCOS and one should select a model most suitable for their purpose. This review will be helpful for consideration of rodent models for PCOS which are not conventionally used to determine mechanisms at the molecular/cellular levels encouraging development of novel treatments and control methods for PCOS.