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. Preeclampsia, a hypertensive disorder unique to pregnancy, is leading cause of maternal and neonatal morbidity and mortality. Endothelial dysfunction is a central feature in the pathophysiology of preeclampsia and mechanisms that have been suggested to contribute to the endothelial dysfunction include hyperinsulinenmia, dyslipidemia, and high cardiac output. Insulin resistance and high cardiac output persist postpartum, suggesting that these women have an underlying disorder. It is unknown whether there is persistence of other features commonly associated with the insulin resistance syndrome and whether these features are linked and contribute to endothelial dysfunction. Thus, the specific aims of this proposal are: 1) Evaluate postpartum women with a history of preeclampsia for features of the insulin resistance syndrome that are thought to contribute to endothelial dysfunction, and 2) Explore the relationships between insulin resistance and these identified features by evaluating for improvement in these abnormalities after insulin resistance is ameliorated with an insulin sensitizing agent. A case-control study, designed to examine specific aim 1, will address the hypothesis that postpartum women with a history of preeclampsia are insulin resistant and have features of the insulin resistance syndrome (central adiposity, dyslipidemia, elevated cardiac output, and decreased endothelial dependent vasodilation) as compared to women without a history of preeclampsia.
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