Interface between reproductive and metabolic dysfunction in polycystic ovary syndrome.

PURPOSE OF REVIEW

New concepts have emerged regarding how interrelationships of hyperandrogenism and hyperinsulinemia from systemic insulin resistance contribute to the origins of polycystic ovary syndrome (PCOS). Although these androgen-insulin interrelationships are associated with several reproductive and metabolic variables, their specific cause and effect relationships remain unclear. This review examines specific causal relationships between hyperandrogenism and hyperinsulinemia from systemic insulin resistance to understand how these complex interactions contribute to the phenotypic expression of PCOS.

RECENT FINDINGS

Clinical interventions for the treatments of hyperandrogenism and hyperinsulinemia from systemic insulin resistance as well as in-vitro studies of androgen and insulin actions on critical target tissues are examined to understand why androgen-insulin interrelationships are central to the origins of PCOS.

SUMMARY

Bidirectional interrelationships between hyperandrogenism and hyperinsulinemia from systemic insulin resistance in normal-weight PCOS women may have originally evolved as an ancient metabolic adaptation to simultaneously favor fat storage and energy utilization for survival and reproduction during famine. These androgen-insulin interactions in PCOS now predispose to metabolic diseases and pregnancy complications in today's obesogenic environment and, therefore, require improved preventive healthcare to optimize the long-term health of PCOS women and their children.