Molecular & genetic factors contributing to insulin resistance in polycystic ovary syndrome.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder of unknown etiology. Insulin resistance is very common and plays a central pathogenic role in PCOS. During last decade several studies have been conducted to understand the mechanisms contributing to the state of insulin resistance and insulin-induced hyperandrogenemia in PCOS. Insulin signaling pathways have been dissected in different insulin responsive tissues such as skeletal muscles, adipose tissues, fibroblasts as well as ovaries to elucidate the mechanism. These studies suggest a post receptor signaling defect where metabolic action of insulin is affected but not the steroidogenic and mitogenic actions. Despite advancement in these studies gaps exist in our understanding of the mechanism of insulin resistance as well as insulin- induced steroidogenesis in PCOS. The syndrome is now considered as a complex multigenic disorder. Efforts are ongoing to dissect the variants of genes from multiple logical pathways which are involved in pathophysiology of the syndrome. But still today no gene has been emerged as universally accepted susceptibility gene for PCOS. This review briefly describes the lacunae along with the current status of molecular events underlying insulin resistance and the contribution of insulin signaling pathway genes in pathogenesis of PCOS along with future researchable areas.
Mukherjee
Sarbani
S
Department of Molecular Endocrinology, National Institute for Research in Reproductive Health (ICMR) Mumbai, India. mukherjees@nirrh.res.in
Maitra
Anurupa
A
D017667:Adipocytes / Q000166:cytology / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000502:physiology; D014644:Genetic Variation; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D018482:Muscle, Skeletal / Q000166:cytology / Q000502:physiology; D011085:Polycystic Ovary Syndrome / Q000209:etiology / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology
D007328:Insulin