Women's HealthPending review
Polycystic ovary syndrome
Insulin resistance drives compensatory hyperinsulinaemia that pushes the ovary to overproduce androgens and arrests follicle development, producing the combination of hyperandrogenism, anovulation and polycystic ovaries.
First principles
Insulin resistance is the metabolic engine of the syndrome
Many women with PCOS have peripheral insulin resistance, and the pancreas compensates by secreting more insulin to keep blood glucose normal. That excess insulin does not stay confined to glucose control: it acts directly on ovarian theca cells to stimulate androgen production, and it suppresses hepatic production of sex hormone-binding globulin (SHBG), raising the proportion of free, biologically active androgen in the circulation.
Educational content pending clinical review. Not medical advice.