Pita M L, Hortelano P, José Faus M, Sánchez-Medina F
Rev Esp Fisiol. 1982 Mar;38(1):21-8.
Renal gluconeogenic capacity was enhanced to 150% 24 h after partial hepatectomy, remained increased at 48 h (144%) and returned to normal values at 72 h. Glucose production by renal cortical slices from hepatectomized rats was also enhanced 48 h after surgery when pyruvate, alpha-ketoglutarate and fructose were used as gluconeogenic precursors. The stimulation of renal gluconeogenic capacity seems to be due to the increase of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities which behaved similarly to glucose production after hepatectomy. The renal metabolic response may be partially due to starvation in the first 24 h. Afterwards food intake became normalized and the acceleration of glucose production should be attributed to hepatectomy. Since there was no metabolic acidosis in our experimental conditions the involvement of glucocorticoids in the stimulation of renal phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities is suggested.
部分肝切除术后24小时,肾脏糖异生能力增强至150%,48小时时仍保持升高(144%),72小时时恢复至正常水平。当使用丙酮酸、α-酮戊二酸和果糖作为糖异生前体时,肝切除大鼠肾皮质切片的葡萄糖生成在术后48小时也增强。肾脏糖异生能力的刺激似乎是由于磷酸烯醇式丙酮酸羧激酶和葡萄糖-6-磷酸酶活性的增加,它们的变化与肝切除术后的葡萄糖生成相似。肾脏的代谢反应可能部分归因于最初24小时的饥饿。之后食物摄入量恢复正常,葡萄糖生成的加速应归因于肝切除。由于在我们的实验条件下没有代谢性酸中毒,提示糖皮质激素参与了对肾脏磷酸烯醇式丙酮酸羧激酶和葡萄糖-6-磷酸酶活性的刺激。