Research Project
2421478
The polycystic ovary syndrome (PCOS) is a prevalent disorder that affects approximately 6% of women of childbearing age. PCOS is characterized by hyperandrogenism and anovulation, and is the major cause of infertility in the United States. Evidence suggests that insulin resistance accompanied by compensatory hyperinsulinemia is a common feature of PCOS, being responsible in part for the hyperandrogenism. Our hypothesis is that an alteration in the post receptor inositol glycan insulin signalling pathway is responsible for the overexpression of the hormone's effects in ovarian tissue. This is manifest as an increased androgen production in PCOS. In previous studies we have demonstrated a defect in the formation of a D-chiroinositol containing glycan mediator in skeletal muscle and an elevated formation of a myoinositol containing mediator in this signalling pathway as a unique feature of metabolic insulin resistance associated with Type ll diabetes in man. We now propose to measure components of this signalling pathway in subjects with PCOS. If our studies demonstrate that an alteration in this intracellular signalling pathway is a characteristic of PCOS, it will provide the means to develop a simple diagnostic test. Furthermore, such information will allow drug therapy to be targeted at correcting the underlying defect. PROPOSED COMMERCIAL APPLICATIONS Development of a diagnostic test and therapeutic approach for the clinical management of polycystic ovary syndrome.
