Conover C A, Rozovski S J, Belur E R, Aoki T T, Ruderman N B
Biochem J. 1980 Nov 15;192(2):725-32. doi: 10.1042/bj1920725.
The activity of ornithine decarboxylase, the rate-controlling enzyme in polyamine biosynthesis, was determined in tissues of normal control rats and rats made diabetic with streptozotocin. In untreated diabetic rats fed ad libitum, ornithine decarboxylase activity was markedly diminished in liver, skeletal muscle, heart and thymus. Ornithine decarboxylase was not diminished in a comparable group of diabetic rats maintained on insulin. Starvation for 48h decreased ornithine decarboxylase activity to very low values in tissues of both normal and diabetic rats. In the normal group, refeeding caused a biphasic increase in liver ornithine decarboxylase; there was a 20-fold increase in activity at 3h followed by a decrease in activity, and a second peak between 9 and 24h. Increases in ornithine decarboxylase in skeletal muscle, heart and thymus were not evident until after 24-48h of refeeding, and only a single increase occurred. The increase in liver ornithine decarboxylase in diabetic rats was greater than in normal rats after 3h of refeeding, but there was no second peak. In peripheral tissues, the increase in ornithine decarboxylase with refeeding was diminished. Skeletal-muscle ornithine decarboxylase is induced more rapidly when meal-fed rats are refed after a period without food. Refeeding these rats after a 48h period without food caused a 5-fold increase in ornithine decarboxylase in skeletal muscle at 3h in control rats but failed to increase activity in diabetic rats. When insulin was administered alone or together with food to the diabetic rats, muscle ornithine decarboxylase increased to activities even higher than in the refed controls. In conclusion, these findings indicate that the regulation of ornithine decarboxylase in many tissues is grossly impaired in diabetes and starvation. They also suggest that polyamine formation in vivo is an integral component of the growth-promoting effect of insulin or some factor dependent on insulin.
测定了正常对照大鼠和用链脲佐菌素诱导糖尿病大鼠组织中鸟氨酸脱羧酶（多胺生物合成中的限速酶）的活性。在自由进食的未治疗糖尿病大鼠中，肝脏、骨骼肌、心脏和胸腺中的鸟氨酸脱羧酶活性显著降低。在接受胰岛素治疗的一组可比糖尿病大鼠中，鸟氨酸脱羧酶活性并未降低。正常和糖尿病大鼠组织经48小时饥饿后，鸟氨酸脱羧酶活性均降至极低水平。在正常组中，重新喂食导致肝脏鸟氨酸脱羧酶呈双相增加；3小时时活性增加20倍，随后活性下降，9至24小时之间出现第二个峰值。骨骼肌、心脏和胸腺中的鸟氨酸脱羧酶直到重新喂食24 - 48小时后才明显增加，且仅出现一次增加。重新喂食3小时后，糖尿病大鼠肝脏中鸟氨酸脱羧酶的增加幅度大于正常大鼠，但没有第二个峰值。在周围组织中，重新喂食后鸟氨酸脱羧酶的增加幅度减小。在一段时间未进食后重新喂食的定时喂食大鼠中，骨骼肌鸟氨酸脱羧酶诱导更快。在48小时未进食后重新喂食这些大鼠，对照组大鼠骨骼肌中鸟氨酸脱羧酶在3小时时增加了5倍，但糖尿病大鼠的活性未增加。当单独或与食物一起给糖尿病大鼠注射胰岛素时，肌肉鸟氨酸脱羧酶增加至甚至高于重新喂食对照组的活性。总之，这些发现表明，糖尿病和饥饿时许多组织中鸟氨酸脱羧酶的调节严重受损。它们还表明，体内多胺的形成是胰岛素或某些依赖胰岛素的因子促进生长作用的一个组成部分。
