GENETICS OF PCOS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The overall aim of this protocol is to test the hypothesis that genetic factors contribute to the failure of the pancreatic ¿-cell to adequately compensate for insulin resistance in polycystic ovary syndrome (PCOS). Insulin resistance is a key factor in the development of type 2 diabetes in PCOS. We have found that insulin secretory defects also play an important role in predisposing this population to diabetes and that a history of type 2 diabetes in a first-degree relative appears to define a subset of PCOS subjects with the most profound defects in ¿-cell function. We have also found that that low-dose glucocorticoid administration may act as a pharmacologic probe to detect subclinical defects in ¿-cell function, thus permitting identification of those at highest risk for developing diabetes. In the present studies we propose to utilize a candidate gene approach to study the genetic basis of insulin secretory dysfunction in PCOS.