Rogers K S, Chan W, Higgins E S
Department of Biochemistry and Molecular Biophysics, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
Biochem Med Metab Biol. 1988 Aug;40(1):46-9. doi: 10.1016/0885-4505(88)90103-x.
Streptozotocin-induced diabetes of 7 weeks duration increased male Sprague-Dawley rat kidney ornithine decarboxylase activity by 4.8-fold but did not affect the liver enzyme. Hydrazine treatment of 4 hr duration stimulated equally kidney ornithine decarboxylase activities of nondiabetic and diabetic rats. Hydrazine treatment increased liver ornithine decarboxylase activity in the nondiabetic rat but did not increase it in the diabetic rat. Since hydrazine stimulates ornithine decarboxylase activity prior to polyamine and protein syntheses, we speculate that the lack of hydrazine stimulation of ornithine decarboxylase in the diabetic liver may be related in part to the unrestrained gluconeogenesis and depressed Kreb's cycle activity: the latter being required for protein synthesis.
持续7周的链脲佐菌素诱导的糖尿病使雄性Sprague-Dawley大鼠肾脏的鸟氨酸脱羧酶活性增加了4.8倍,但对肝脏中的该酶没有影响。持续4小时的肼处理同样刺激了非糖尿病和糖尿病大鼠肾脏中的鸟氨酸脱羧酶活性。肼处理增加了非糖尿病大鼠肝脏中的鸟氨酸脱羧酶活性,但在糖尿病大鼠中未增加。由于肼在多胺和蛋白质合成之前刺激鸟氨酸脱羧酶活性,我们推测糖尿病肝脏中鸟氨酸脱羧酶缺乏肼刺激可能部分与不受抑制的糖异生和Krebs循环活性降低有关:后者是蛋白质合成所必需的。