ENERGY-METABOLISM IN HYPOXIC ASTROCYTES - PROTECTIVE MECHANISM OF FRUCTOSE-1,6-BISPHOSPHATE

ENERGY-METABOLISM IN HYPOXIC ASTROCYTES - PROTECTIVE MECHANISM OF FRUCTOSE-1,6-BISPHOSPHATE
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DOI:
10.1007/bf00969690
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发表时间:
1995-07-01
影响因子:
4.4
通讯作者:
GREGORY, GA
GREGORY, GA
中科院分区:
医学3区
文献类型:
--
作者:
KELLEHER, JA;CHAN, PH;GREGORY, GA

文献摘要

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1,6-二磷酸果糖 (FBP) 在缺氧/缺血期间的保护作用被认为是由于摄取和利用 FBP 作为糖酵解底物或刺激葡萄糖代谢所致。为了检验这些假设,我们测量了常氧和低氧培养的星形胶质细胞中存在和不存在 FBP 的情况下,[6-C-14] 葡萄糖、[1-C-14] 葡萄糖和 [U-C-14]FBP 产生的 CO2 和乳酸。 FBP对糖酵解产生的CO2影响不大,但增加了磷酸戊糖途径产生的CO2。标记的 FBP 产生极少量的 CO2。在低氧缺氧期间,[1-和6-C-14]葡萄糖产生的乳酸同样增加;该增加与添加的 FBP 无关。 [U-C-14]FBP 中标记的乳酸极少。我们得出的结论是,星形胶质细胞不使用外源性 FBP 作为糖酵解的底物,并且 FBP 会改变葡萄糖代谢。
The protective effects of fructose-1,6-biphosphate (FBP) during hypoxia/ischemia are thought to result from uptake and utilization of FBP as a substrate for glycolysis or from stimulation of glucose metabolism. To test these hypotheses, we measured CO2 and lactate production from [6-C-14]glucose, [1-C-14]glucose, and [U-C-14]FBP in normoxic and hypoxic cultured astrocytes with and without FBP present. FBP had little effect on CO2 production by glycolysis, but increased CO2 production by the pentose phosphate pathway. Labeled FBP produced very small amounts of CO2. Lactate production from [1-, and 6-C-14]glucose increased similarly during hypoxic hypoxia; the increase was independent of added FBP. Labeled lactate from [U-C-14]FBP was minimal. We conclude that exogenous FBP is not used by astrocytes as a substrate for glycolysis and that FBP alters glucose metabolism.