INSULIN SECRETION FROM PANCREATIC ISLET BETA CELLS

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 还原当量、NAD（P）H和NADH在胰岛细胞分泌胰岛素的调节中起重要作用。在这一过程中，细胞溶质和线粒体代谢以及两个库中还原当量的变化都是重要因素。 为了进一步阐明胞浆和线粒体组分的作用，我一直在研究整个小鼠和大鼠胰岛对胰岛素分泌物、葡萄糖和线粒体底物琥珀酸的NAD（P）H反应，使用Zeiss LSM共聚焦显微镜，配备了我用来激发NAD（P）H的双光子激光。 这项工作是在彼得·史密斯博士作为研究助理科学家加入该小组之前，在生物电流研究中心的实验室中作为心脏博士草奖学金的一部分完成的。 在奖学金项目中，Emma能够收集显示线粒体燃料琥珀酸对大鼠和小鼠中NAD（P）H水平的差异影响的数据，这些大鼠和小鼠具有不同程度的细胞溶质与线粒体代谢。这项工作将有助于了解胰岛素分泌的分子机制，以不同的胰岛素secretaqoques，并最终损害，如果这种功能在2型糖尿病的条件。

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.