ENDOTOXIN CAUSES RECIPROCAL CHANGES IN HEPATIC NITRIC-OXIDE SYNTHESIS, GLUCONEOGENESIS, AND FLUX THROUGH PHOSPHOENOLPYRUVATE CARBOXYKINASE
ENDOTOXIN CAUSES RECIPROCAL CHANGES IN HEPATIC NITRIC-OXIDE SYNTHESIS, GLUCONEOGENESIS, AND FLUX THROUGH PHOSPHOENOLPYRUVATE CARBOXYKINASE
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DOI：
10.1006/bbrc.1994.2510
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发表时间：
1994-10-28
影响因子：
3.1
通讯作者：
TITHERADGE, MA
中科院分区：
文献类型：
--
作者：
HORTON, RA;KNOWLES, RG;TITHERADGE, MA
用细菌内毒素治疗大鼠，3小时内可显着诱导肝一氧化氮合酶。反应在 12 小时时达到最大，并维持超过 18 小时。一氧化氮合酶的诱导与血浆硝酸盐和亚硝酸盐浓度的增加以及随后分离的肝细胞中葡萄糖合成的抑制密切相关。糖异生速率的下降也与通过磷酸烯醇丙酮酸羧激酶的通量的抑制相关，但与通过丙酮酸激酶或6-磷酸果糖-1-激酶的通量的改变无关，这表明一氧化氮诱导的磷酸烯醇丙酮酸羧激酶的抑制可能是脓毒症中葡萄糖产生减少的基础。 (C) 1994 年学术出版社
Treatment of rats with bacterial endotoxin resulted in a significant induction of hepatic nitric oxide synthase within 3 hours. The response was maximal at 12 hours and was maintained over 18 hours. The induction of nitric oxide synthase correlated well with the increase in plasma nitrate plus nitrite concentrations and also with the inhibition of glucose synthesis in subsequently isolated hepatocytes. The decline in the rate of gluconeogenesis also correlated with an inhibition of flux through phosphoenolpyruvate carboxykinase but not with alterations in flux through either pyruvate kinase or 6-phosphofructo-1-kinase, suggesting that a nitric oxide-induced inhibition of phosphoenolpyruvate carboxykinase may underlie the decreased glucose production in sepsis. (C) 1994 Academic Press, Inc.