Molecular mechanisms of insulin resistance in polycystic ovary syndrome

Trends Mol Med. 2006 Jul;12(7):324-32. doi: 10.1016/j.molmed.2006.05.006.


Polycystic ovary syndrome (PCOS) is a common endocrinopathy of unknown aetiology that affects women of reproductive age. During the past ten years, defective insulin activity in PCOS has been demonstrated in target tissues and causes insulin resistance and hyperinsulinaemia. Furthermore, presence of insulin receptors in the ovarian tissue and overproduction of androgens by theca cells leads to characteristic hyperandrogenaemia. Recent data suggest a divergence in post-receptor signalling pathways for insulin in its target tissues (muscle, adipocytes and ovarian tissue), where the metabolic pathway of insulin activity is defective, whereas the activation of steroidogenesis is maintained. Investigators are still searching for clues to understand the cause of this enigmatic syndrome, despite great advances in molecular medicine and genetics.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Female
  • Fibroblasts / metabolism
  • Humans
  • Hyperandrogenism / physiopathology
  • Insulin / metabolism
  • Insulin Resistance / physiology*
  • Muscle, Skeletal / physiopathology*
  • Ovary / physiopathology*
  • Polycystic Ovary Syndrome / physiopathology*
  • Signal Transduction


  • Insulin