REGULATION OF GLUCOSE TRANSPORT IN THE ISCHEMIC HEART

描述（改编自申请人的描述）：缺血产生 葡萄糖转运蛋白GLUT4和GLUT1易位到 肌膜是对能量需求的关键反应。本研究建议， 了解这种反应的机制，通过使用大鼠乳头肌， 结合药理学工具和犬缺血的体内模型。 待检验的假设是缺血触发AMP激酶的激活， 一种细胞内蛋白质，被认为能增加葡萄糖转运蛋白， 肌膜AMPK与其他信号通路的相互作用将是 探索，以及AMPK亚基的特定亚型在 心胞吐作用与胞吞作用在该过程中的相对作用将是 评估。

DESCRIPTION (adapted from the applicant's description): Ischemia produces translocation of the glucose transport proteins GLUT4 and GLUT1 to the sarcolemma as a critical response to a need for energy. This study proposes to understand the mechanism of this response by using rat papillary muscle in combination with pharmacological tools and an in vivo model of canine ischemia. The hypothesis to be tested is that ischemia triggers activation of AMP kinase, an intracellular protein that is proposed to increase glucose transporters on the sarcolemma. Interaction of AMPK with other signaling pathways will be explored, as well as the role of specific isoforms of AMPK subunits in the heart. The relative roles of exocytosis vs. endocytosis in the process will be evaluated.