GLUCOSE/FUEL METABOLISM & CALCIUM IN PANCREATIC ISLETS

该项目的长期目标是继续研究 胰岛素刺激-分泌偶联中糖代谢与钙 分泌物 葡萄糖是最有效的胰岛素促分泌剂，钙是 被认为是胰腺β细胞内重要的信使， cell. 初步证据表明钙可能影响葡萄糖代谢， 收缩蛋白、蛋白磷酸化和磷脂代谢 在胰腺中，在胰岛中，以及它们之间的关系， 因素将被追究。 线粒体甘油磷酸脱氢酶是 一种在大鼠胰岛中高度活跃的钙激活酶 该酶被二氮嗪和胰岛素抑制剂抑制 release. 在人胰岛素分泌组织中研究这种酶将是 持续期间内的 将继续进行研究，旨在提供线索， 葡萄糖是否刺激了蛋白质磷酸化的可辨别模式 完整胰岛中磷脂代谢以及钙如何介导 这些过程。 收缩蛋白可能为胰岛素颗粒运动提供动力 在beta细胞中。 胰岛含有肌球蛋白轻链激酶， 一种钙-钙调蛋白激活酶，催化 平滑肌肌球蛋白使肌球蛋白ATP酶被肌动蛋白激活， 收缩可以发生。 计划进行研究以部分表征 胰岛中的钙激活蛋白激酶，包括那些可能 催化肌球蛋白磷酸化。 青少年（I型）糖尿病是由于β细胞缺乏引起的胰岛素缺乏症。 破坏或故障。 病理过程是否起源于 β细胞或身体其他部位是未知的。 可疑原因 成人型（II型）糖尿病包括胰岛素抵抗，其中胰岛素抵抗是指胰岛素抵抗。 β细胞的生产无法跟上身体的步伐。 需要，以及β细胞的原发性代谢异常。 由于这些疾病中β细胞功能障碍的确切原因是 未知，任何旨在阐明正常生理学的研究 β细胞是重要的，在了解其病理生理。 此外，本发明还提供了一种方法， 更好地了解β细胞代谢可能有助于 研究人员有兴趣在组织培养中保存β细胞， 治疗目的，如移植。

The project's long term objective is to continue research on the role of glucose metabolism and calcium in stimulus-secretion coupling in insulin secretion. Glucose is the most potent insulin secretagogue and calcium is believed to be and important intracellular messenger in the pancreatic beta cell. Preliminary evidence that calcium may influence glucose metabolism, contractile proteins, protein phosphorylation and phospholipid metabolism in pancreatic in pancreatic islets and the relationships between these factors will be pursued. Mitochondrial glycerol phosphate dehydrogenase is a calcium-activated enzyme that is highly active in rat pancreatic islets and the enzyme is inhibited by diazoxide, and inhibitor of insulin release. Studies of this enzyme in human insulin secreting tissues will be continued. Studies will be continued that are designed to give clues about whether glucose stimulates discernable patterns of protein phosphorylation and of phospholipid metabolism in intact islets and how calcium may mediate these processes. Contractile proteins may power insulin granule movements within the beta cell. Pancreatic islets contain myosin light chain kinase, a calcium-calmodulin-activated enzyme that catalyzes phosphorylation of smooth muscle myosin enabling myosin ATPase to be activated by actin so contraction can occur. Studies are planned to partially characterize calcium-activated protein kinases in islets, including those that may catalyze phosphorylation of myosin. Juvenile (Type I) diabetes is caused by insulin deficiency due to beta cell destruction or malfunction. Whether the pathologic process originates in the beta cell or elsewhere in the body is unknown. Suspected causes of adult-onset (Type II) diabetes include insulin resistance, in which insulin production by the beta cell is unable to keep pace with the body's requirements, and also primary metabolic abnormalities of the beta cell. Since the exact causes of beta cell malfunction in these disorders are unknown, any research directed at elucidating the normal physiology of the beta cell is important in understanding its pathophysiology. In addition, a better understanding of beta cell metabolism may be helpful to researchers interested in preserving beta cells in tissue culture for therapeutic purposes, such as transplantation.