Insulin resistance plays a central role in the pathophysiology of PCOS. Which statement best describes its effect?

Answer: B. Hyperinsulinaemia stimulates ovarian androgen secretion and lowers sex hormone-binding globulin, increasing free androgens

Insulin resistance in PCOS

Insulin resistance with compensatory hyperinsulinaemia is central to PCOS and is present in 50-70% of affected women (higher and more severe in South Asians).

How it drives PCOS

• Insulin is a potent stimulus for ovarian androgen secretion and amplifies the effect of LH on theca cells.
• It suppresses hepatic production of sex hormone-binding globulin (SHBG), raising free (active) androgen levels.
• The resulting hyperandrogenism arrests follicular growth, causing anovulation.

Clinical relevance

This explains why weight loss and insulin-sensitising measures improve PCOS - reducing insulin lowers androgens, raises SHBG and can restore ovulation.

Why the others are wrong

Insulin stimulates (not suppresses) androgen production; it lowers (not raises) SHBG, increasing free testosterone; it clearly affects androgens; and insulin resistance is common (50-70%), not rare.