Suzuki T, Ferris R K, Gordon E E
Endocrinology. 1975 Oct;97(4):1058-60. doi: 10.1210/endo-97-4-1058.
Renal as well as hepatic gluconeogenesis is inappropriately accelerated in the diabetic state when plasma glucose levels are elevated. Known regulatory mechanisms influence gluconeogenesis in both organs. However, under certain circumstances gluconeogenesis may be affected in one organ and not the other. Recent studies with the tryptophan metabolite, quinolinate, suggest that hepatic gluconeogenesis in the diabetic is unaffected by this agent, whereas gluconeogenesis is blocked in the normal liver. These experiments have been interpreted as providing evidence for the lack of a specific physiologic repressor for gluconeogenesis in diabetic liver. In the present study quinolinate and hydrazine are shown to be effective inhibitors of the accelerated gluconeogenesis in the renal cortex of diabetic rats. Thus, the renal gluconeogenic mechanism in diabetics retains the capacity to recognize quinolinate as an inhibitor, but may be influenced by the depressed conversion of tryptophan to quinolinate in the intact diabetic organism.
当血浆葡萄糖水平升高时，糖尿病状态下肾和肝的糖异生都会不适当加速。已知的调节机制影响这两个器官的糖异生。然而，在某些情况下，一个器官的糖异生可能受到影响而另一个器官不受影响。最近关于色氨酸代谢产物喹啉酸的研究表明，糖尿病患者肝脏的糖异生不受该物质影响，而正常肝脏中的糖异生则被阻断。这些实验被解释为提供了证据，证明糖尿病肝脏中缺乏糖异生的特异性生理抑制剂。在本研究中，喹啉酸和肼被证明是糖尿病大鼠肾皮质中加速糖异生的有效抑制剂。因此，糖尿病患者的肾糖异生机制仍有能力将喹啉酸识别为抑制剂，但可能会受到完整糖尿病机体中色氨酸向喹啉酸转化降低的影响。
