Van Noorden C J, Döpp E A, Dijkstra C D, Aronson D C, Lamers W H, De Graaf A, Frederiks W M
Laboratory of Histology and Cell Biology, University of Amsterdam, The Netherlands.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1988;54(4):252-5. doi: 10.1007/BF02899219.
The effect of experimentally induced cholestasis on the amount of phosphoenolpyruvate carboxykinase (PEPCK) was studied immunohistochemically in rat liver parenchyma. In control liver, the enzyme was mainly localized periportally and, although the enzyme content was much reduced, this distribution pattern was maintained up to 2 weeks after ligation of the common bile duct. At 4 and 8 weeks after ligation the enzyme content in parenchymal cells remained low, but became distributed homogeneously throughout the liver parenchyma. This suggests that after bile duct ligation, gluconeogenesis from lactate is impaired. This may well be the cause of the adaptive changes to enhance the glycogenolytic capacity of parenchymal cells to maintain as far as possible a constant blood glucose level.
通过免疫组织化学方法研究了实验性诱导胆汁淤积对大鼠肝实质中磷酸烯醇丙酮酸羧激酶(PEPCK)含量的影响。在对照肝脏中,该酶主要定位于门静脉周围,并且尽管酶含量大幅降低,但在胆总管结扎后长达2周这种分布模式仍得以维持。结扎后4周和8周时,实质细胞中的酶含量仍然很低,但在整个肝实质中呈均匀分布。这表明胆管结扎后,由乳酸生成葡萄糖的糖异生作用受到损害。这很可能是实质细胞糖原分解能力增强以尽可能维持血糖水平恒定的适应性变化的原因。