INSULIN SECRETION FROM PANCREATIC ISLET BETA CELLS

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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. Reducing equivalents, NAD(P)H and NADH play important roles in regulation of insulin secretion from pancreatic islet cells. Both cytosolic and mitochondrial metabolism and resulting changes in reducing equivalents in both pools are important factors in this process. To further elucidate the role of cytosolic and mitochondrial components, I have been studying NAD(P)H responses of whole mouse and rat pancreatic islets to insulin secretaqoques, glucose and the exclusive mitochondrial substrate succinate, using Zeiss LSM confocal microscope equipped with 2-photon laser which I have used for excitation of NAD(P)H. This work was done as a part of Dr Heart's Grass Fellowship in the lab of Dr. Peter Smith at the BioCurrents Research Center, prior to her joining the group as a Research Assistant Scientist. In the fellowship project Emma was able to collect data showing differential effect of mitochondrial fuel succinate on NAD(P)H levels in rat and mouse, which have a different degree of cytosolic versus mitochondrial metabolism. This work will help in understanding the molecular mechanism underlying insulin secretion to different insulin secretaqoques and ultimately impairment if this function in the type 2 diabetic conditions.