Figure 1.

Proposed pathogenic mechanisms in obesity-associated ovarian dysfunction and subfertility. Schematic showing the major metabolic and reproductive pathways involved in PCOS. Systemic insulin resistance, commonly due to adipose tissue dysfunction in the context of obesity, results in compensatory hyperinsulinemia. At the ovary, insulin synergizes with luteinizing hormone (LH) to drive androgen synthesis. Disrupted insulin, growth factor, gonadotrophin, and sex steroid signaling in the ovary leads to failure of follicle development and ovulation. Genetic and developmental influences are also likely to play an important role.