REGULATION OF GLUCOSE TRANSPORT IN THE ISCHEMIC HEART

描述(改编自申请者的描述)：缺血产生 葡萄糖转运蛋白GLUT4和GLUT1转位到 作为对能量需求的关键反应的肌膜。这项研究建议 用大鼠乳头肌的方法研究这种反应的机制。 结合药理工具和犬在体缺血模型。 需要检验的假设是，缺血触发了AMP激酶的激活， 一种细胞内蛋白质，被认为可以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 以及特定的AMPK亚基的作用。 心。胞吐作用和内吞作用在这一过程中的相对作用如下 已评估。

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.