Appel M C, Like A A, Rossini A A, Carp D B, Miller T B
Am J Physiol. 1981 Feb;240(2):E83-7. doi: 10.1152/ajpendo.1981.240.2.E83.
The effects of diabetes on hepatic carbohydrate metabolism were investigated in spontaneously diabetic Bio-Breeding Worcester (BB/W) rats. The juvenile-onset-type syndrome displayed by these animals is characterized by beta-cell destruction with subsequent ketosis-prone insulinopenia. Livers from diabetic animals demonstrated increased adenosine 3',5'-cyclic monophosphate levels but subnormal total protein and glycogen content. Isolated perfused livers of diabetic BB/W rats demonstrated an increased rate of glucose production from [14C]lactate and an impaired rate of glycogen synthesis. These data were consonant with hepatic enzyme studies demonstrating markedly increased activities of component gluconeogenic (glucose-6-phosphatase, fructose-1,6-diphosphatase, phosphoenolpyruvate carboxykinase) and glycogenolytic (glycogen phosphorylase) enzymes with decreased activities of glycolytic (hexokinase, pyruvate kinase) and glycogenic (glycogen synthase) enzymes. These findings agree with previous studies using alloxan- and streptozotocin-induced diabetic animals and suggest that accelerated hepatic gluconeogenesis and impaired glucose utilization are pathognomonic of all insulin-deficient diabetic syndromes.
在自发性糖尿病的Bio-Breeding Worcester（BB/W）大鼠中研究了糖尿病对肝脏碳水化合物代谢的影响。这些动物表现出的青少年发病型综合征的特征是β细胞破坏，随后出现易发生酮症的胰岛素缺乏。糖尿病动物的肝脏显示出3',5'-环磷酸腺苷水平升高，但总蛋白和糖原含量低于正常水平。糖尿病BB/W大鼠的离体灌注肝脏显示，[14C]乳酸生成葡萄糖的速率增加，糖原合成速率受损。这些数据与肝脏酶研究结果一致，该研究表明糖异生（葡萄糖-6-磷酸酶、果糖-1,6-二磷酸酶、磷酸烯醇丙酮酸羧激酶）和糖原分解（糖原磷酸化酶）酶的活性显著增加，而糖酵解（己糖激酶、丙酮酸激酶）和糖原生成（糖原合酶）酶的活性降低。这些发现与先前使用四氧嘧啶和链脲佐菌素诱导的糖尿病动物的研究结果一致，并表明肝脏糖异生加速和葡萄糖利用受损是所有胰岛素缺乏性糖尿病综合征的特征。
