Insulin resistance
When cells respond less to insulin, the pancreas releases more to do the same job. In PMOS, this loops with ovarian androgen production.
Insulin resistance is when cells respond less to insulin. To do the same job, moving glucose out of the bloodstream and into cells where it can be used, the pancreas releases more insulin. The amount circulating goes up. The cells stay sluggish.
This matters in PMOS because the ovaries do not become resistant in the same way muscle and fat tissue do. They keep listening. When insulin in circulation is elevated, the ovaries respond by producing more androgens. That is the mechanism behind the insulin-androgen loop: high insulin nudges ovarian androgen production, the androgens make insulin resistance worse, the loop perpetuates.
Insulin resistance is documented in approximately 85% of people with PMOS overall, and around 75% of people with PMOS at a lean body weight (2026 Lancet consensus). It is the metabolic core of the condition.
Standard fasting glucose tests usually miss it. By the time fasting glucose has moved out of the normal range, insulin resistance has often been present for years. HOMA-IR or fasting insulin is more sensitive.