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首页> 外文期刊>American Journal of Physiology >Ischemia-induced activation of AMPK does not increase glucose uptake in glycogen-replete isolated working rat hearts
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Ischemia-induced activation of AMPK does not increase glucose uptake in glycogen-replete isolated working rat hearts

机译:缺血诱导的AMPK激活不会增加糖原充足的离体大鼠心脏的葡萄糖摄取

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摘要

Several studies have investigated ischemia-induced alterations in glucose uptake, but these have yielded conflicting conclusions. More than three decades ago, Neely and colleagues (35, 37) showed that ischemia reduces glucose uptake and glycolysis. However, those results contrast with positron emission tomography studies that show an increase in the uptake of 18F-deoxyglucose in relation to coronary flow in patients with coronary artery disease (10, 32). Similar observations in vivo (50) and ex vivo (40, 45) were attributed to a translocation of GLUT4 to the cell surface, due to ischemia-induced activation of adenosine 5'-monophosphate-activated protein kinase (AMPK) (39).
机译:几项研究研究了缺血引起的葡萄糖摄取改变,但得出了矛盾的结论。三十多年前,Neely及其同事(35、37)表明,局部缺血可减少葡萄糖摄取和糖酵解。但是,这些结果与正电子发射断层扫描研究相反,正电子发射断层扫描研究显示,与冠状动脉疾病患者的冠脉流量相关的18 F-脱氧葡萄糖摄取量有所增加(10、32)。由于缺血诱导的腺苷5'-单磷酸激活蛋白激酶(AMPK)的激活,体内(50)和离体(40,45)的类似观察结果归因于GLUT4易位至细胞表面(39)。

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