Hyperandrogenism is known to be associated with polycystic ovarian (or ovary) syndrome. In this disease, ovarian follicles proliferate in a dysregulated fashion – in part due to excess androgen signaling within the ovary itself – leading to anovulation and infertility. Intriguingly, while excess androgen signaling in the ovary promotes unregulated follicle growth, a certain level of androgen signaling appears to be required for normal follicular development. In fact, deficient androgen signaling in the ovary might lead to premature ovarian failure, another cause of female infertility. This article discusses various in vitro and animal models being used to study the pathophysiology of hyper- and hypoandrogenism, focusing on the role of androgens and androgen receptor-mediated actions in normal and pathologic ovarian physiology.