Soler C, Cragoe E J, Soley M
Departament de Bioquímica i Fisiologia, Universitat de Barcelona, Spain.
Regul Pept. 1994 Jun 16;52(1):1-6. doi: 10.1016/0167-0115(94)90015-9.
Epidermal growth factor (EGF) triggers rapid and delayed effects on gluconeogenesis, cytosolic (lactate/pyruvate ratio) and mitochondrial (3-hydroxybutyrate/acetoacetate ratio) redox states (Soler, C. and Soley, M., Biochem. J., 294 (1993) 865-872). This study attempts to determine whether the mechanism by which EGF modulates any of these parameters is dependent on the regulation of Na+/H+ exchange and/or Na+/K(+)-ATPase activities. The Na+/H+ exchange was inhibited by either amiloride or the analogue 5-(N,N-hexamethylene)amiloride (HMA), and the Na+/K(+)-ATPase activity was inhibited by ouabain. The delayed EGF inhibition of gluconeogenesis, increase of the lactate/pyruvate ratio and decrease in the 3-hydroxybutyrate/acetoacetate ratio were unaltered in the presence of amiloride, HMA or ouabain. The rapid EGF stimulation of gluconeogenesis was also observed in the presence of HMA or ouabain. Although Na+/H+ exchange and/or Na+/K(+)-ATPase are regulated by EGF, our results indicate that these activities are not required for the effects of EGF on gluconeogenesis and/or cytosolic and mitochondrial redox state.
表皮生长因子（EGF）对糖异生、胞质（乳酸/丙酮酸比值）和线粒体（3-羟基丁酸/乙酰乙酸比值）氧化还原状态产生快速和延迟效应（索勒，C.和索利，M.，《生物化学杂志》，294（1993）865 - 872）。本研究试图确定EGF调节这些参数的机制是否依赖于钠/氢交换和/或钠/钾-ATP酶活性的调节。钠/氢交换被氨氯吡咪或类似物5 -（N，N - 六亚甲基）氨氯吡咪（HMA）抑制，钠/钾-ATP酶活性被哇巴因抑制。在存在氨氯吡咪、HMA或哇巴因的情况下，EGF对糖异生的延迟抑制、乳酸/丙酮酸比值的增加以及3-羟基丁酸/乙酰乙酸比值的降低均未改变。在存在HMA或哇巴因的情况下也观察到了EGF对糖异生的快速刺激。尽管钠/氢交换和/或钠/钾-ATP酶受EGF调节，但我们的结果表明，这些活性并非EGF对糖异生和/或胞质及线粒体氧化还原状态产生作用所必需。
