Hanley R M, Strada S J, Steiner A L, Thompson W J, Shenolikar S
Mol Cell Endocrinol. 1987 Mar;50(1-2):115-22. doi: 10.1016/0303-7207(87)90083-9.
Two broad-specifically protein phosphatases, termed protein phosphatase-1 (PrP-1) and protein phosphatase-2A (PrP-2A), accounting for all the hepatic activity regulating glycogen phosphorylase, were measured in spontaneously diabetic Chinese hamsters exhibiting persistent glycosuria. When compared with genetically related inbred sublines free of glycosuria, diabetic animals demonstrated approximately 25% increase in PrP-1 activity measured either in crude tissue extracts or in cytosols fractionated by ion-exchange chromatography. No significant alteration in total PrP-2A activity was observed in the diabetic animals. These findings indicate that a specific change in hepatic PrP-1 is associated with genetically acquired diabetes in Chinese hamsters. In contrast to reported data using animals with experimentally induced diabetes mellitus, hepatic PrP-1 was increased in the spontaneously diabetic Chinese hamsters. The data suggests that distinct alterations in PrP-1 and associated metabolic consequences are exhibited by different types of diabetes.
在表现出持续性糖尿的自发性糖尿病中国仓鼠中，检测了两种广泛特异性蛋白磷酸酶，即蛋白磷酸酶-1（PrP-1）和蛋白磷酸酶-2A（PrP-2A），它们占调节糖原磷酸化酶的所有肝脏活性。与无糖尿的遗传相关近交亚系相比，糖尿病动物在粗组织提取物或通过离子交换色谱分离的胞质溶胶中测得的PrP-1活性增加了约25%。在糖尿病动物中未观察到总PrP-2A活性有显著变化。这些发现表明，肝脏PrP-1的特定变化与中国仓鼠的遗传性糖尿病有关。与使用实验性诱导糖尿病动物的报道数据相反，自发性糖尿病中国仓鼠的肝脏PrP-1增加。数据表明，不同类型的糖尿病表现出PrP-1的明显改变及相关的代谢后果。
