Polycystic ovary syndrome (PCOS) is the most common cause of
female infertility affecting 6-8% of women worldwide. PCOS is characterized by two of the following three criteria: clinical or biochemical
hyperandrogenism, oligo- or
amenorrhea, and polycystic ovaries (PCO). In addition, women with PCOS are often obese and
insulin resistant, and are at risk for
type 2 diabetes and
cardiovascular disease. The etiology of PCOS remains unknown. Therefore, several animal models for PCOS have been generated to gain insight into the etiology and development of the PCOS-associated phenotypes.
Androgens are considered the main culprit of PCOS, and therefore,
androgenization of animals is the most frequently used approach to induce symptoms that resemble PCOS. Prenatal or prepubertal
androgen treatment results in many characteristics of human PCOS, including
anovulation,
cyst-like follicles, elevated
luteinizing hormone (LH) levels, increased adiposity, and
insulin insensitivity. However, PCOS has a heterogeneous presentation, and therefore it is difficult to generate a model that exactly reproduces the reproductive and metabolic phenotypes observed in women with PCOS. In this review, we discuss several mouse models for PCOS, and compare the reproductive and/or metabolic phenotypes observed in several
androgen-induced models as well as in several genetic models.