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 specific aims of our study will be to: 1. Determine the circadian rhythm of PAI-1 in the GHD population prior to and following appropriate replacement with hGH. We hypothesize that the levels of GH and PAI-1 will be inversely related within a normal individual. Additionally, since a GHD individual would lose their circadian secretion of GH, we hypothesize that their PAI-1 level would be chronically high while not on hGH replacement and chronically low once adequately replaced. 2. Evaluate the fibrinolytic potential of patients with GHD prior to and following replacement with hGH. We hypothesize that there will be a defective fibrinolytic response in GHD adults following the venous occlusion test, and that this effect will be abolished following adequate replacement therapy. 3. Evaluate endothelial dysfunction in patients with GHD prior to and following replacement with hGH. We hypothesize that flow-mediated dilation (FMD) will be less prominent in patients with GHD and we hypothesize that flow-mediated dilation will return to baseline following replacement therapy with hGH. 4. Compare, using proteomics, the plasma signature of proteins present in GHD individuals prior to and following replacement therapy with hGH. The absence or presence of different proteins present in the deficient versus the replaced state could only serve to raise further questions regarding the role of GH in inflammation and the pathogenesis of atherosclerosis that may warrant investigation in the future.
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