STUDIES ON THE MECHANISM BY WHICH GLUTAMINE AND HEAT-SHOCK INCREASE LACTATE SYNTHESIS BY L929 CELLS IN THE PRESENCE OF INSULIN
STUDIES ON THE MECHANISM BY WHICH GLUTAMINE AND HEAT-SHOCK INCREASE LACTATE SYNTHESIS BY L929 CELLS IN THE PRESENCE OF INSULIN
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DOI：
10.1002/jcp.1041290317
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发表时间：
1986-12-01
影响因子：
5.6
通讯作者：
LANKS, KW
中科院分区：
文献类型：
--
作者：
LANKS, KW
谷氨酰胺和热休克都增加了L929细胞系统中乳酸的产生。谷氨酰胺现在显示在胰岛素存在下增加己糖摄取，抑制丙酮酸氧化，并向胞质隔室提供还原当量。这些过程对乳酸生产的相对贡献取决于丙酮酸的可用性。当从培养基中获得充足的丙酮酸时，谷氨酰胺和热休克对乳酸合成的刺激是转氨酶依赖性的，这表明涉及还原当量从线粒体到细胞质的穿梭。在不存在培养基丙酮酸的情况下，谷氨酰胺和热休克对糖酵解的刺激在很大程度上是乳酸合成增加的原因。观察到的谷氨酰胺效应似乎都不足以解释观察到的糖酵解刺激。
Both glutamine and heat shock increase lactate production in the L929 cell system. Glutamine is now shown to increase hexose uptake in the presence of insulin, to inhibit puyruvate oxidation, and to provide reducing equivalents to the cytosolic compartment. The relative contribution of these processes to lactate production depends on the availability of pyruvate. When ample pyruvate is available from the culture medium, stimulation of lactate synthesis by glutamine and heat shock is transaminase dependent, suggesting that shuttling of reducing equivalents from mitochondria to cytoplasm is involved. In the absence of medium pyruvate, stimulation of glycolysis by both glutamine and heat shock is largely responsible for increased lactate synthesis. None of the observed effects of glutamine appears to be sufficient to explain the observed stimulation of glycolysis.