Prenatal or postnatal exposure to androgens results in most of the features of PCOS in rodent, sheep, and non-human primate models, including the presence of hyperandrogenemia, oligo- or anovulation and disrupted reproductive cycling, subfertility, elevated LH and altered LH pulsatility, obesity, dyslipidemia, fatty liver, glucose intolerance and insulin resistance, and altered adipokine secretion [19–36]. The gene discussed is PLOD1; the disease is metabolic syndrome.