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. This study is supported by a GCRC student award. It is focused upon one of the subprojects of a previously approved IRB protocol (12681). It focuses upon one aspect of subproject 4 of that proposal. Insulin resistance (IR) is a well-known component of Type 2 diabetes and cardiovascular disease. However, short-term IR is a necessary physiological phenomenon in states such as pregnancy. Maintenance of normal glucose levels during IR is dependent upon the ability of the insulin-secreting beta cells to increase their output in order to overcome the resistance to insulin action that occurs in IR. This proposal will study the physiology of the compensatory increase in insulin secretion in IR. The signal to the beta cells to increase insulin secretion during IR is not well defined;though thought to be glucose, there is reason to suspect that glucose is only part of the mechanism, if at all. The possibility of alternative signaling, beta cell compensatory factors (BCCF) will be studied using the physiological phenomenon of spontaneous IR of pregnancy and comparing it to an experimental model of short-term, drug-induced IR. In addition, preliminary studies of proteomics will be used to initiate identification of potentially new BCCF molecules. Understanding signals for beta cell compensation to IR may lead to new therapeutic possibilities for the prevention or treatment of Type 2 diabetes.
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