Krähenbühl S, Reichen J
Department of Clinical Pharmacology, University of Berne, Switzerland.
J Hepatol. 1993 Aug;19(1):64-70. doi: 10.1016/s0168-8278(05)80177-1.
Energy metabolism was studied in fed and fasted rats with carbon tetrachloride (CCl4)-induced cirrhosis. In situ liver perfusion experiments were performed under basal conditions (no substrate added to the perfusate) and after stimulation with glucagon (2 nM) and L-alanine (20 mM). Under basal conditions, oxygen consumption per gram of liver was reduced in cirrhotic rats irrespective of the metabolic state. After addition of glucagon/L-alanine to the perfusate, oxygen consumption increased significantly in fed and fasted control and cirrhotic rats. Under basal conditions, glucose production was reduced by 76% in cirrhotic rats, averaging 0.75 +/- 0.19 vs. 0.18 +/- 0.15 mumol.g liver-1.min-1 in control and cirrhotic livers, respectively (means +/- S.E.M., P < 0.05). After addition of glucagon/L-alanine to the perfusate, glucose production increased in both groups and was reduced by 65% in fed cirrhotic as compared with fed control rats, averaging 3.63 +/- 0.27 vs. 1.27 +/- 0.17 mumol.g liver-1.min-1 in control and cirrhotic rats, respectively (P < 0.05). Stimulated glucose production was linearly correlated with the fractional aminopyrine elimination rate constant (ABT-k), a measure of hepatic function in vivo. After 12 h of fasting, stimulated glucose production was decreased by 15% in control and by 65% in fed cirrhotic rats compared with the fed state, averaging 3.07 +/- 0.22 vs. 0.33 +/- 0.03 mumol.g liver-1.min-1 in control and cirrhotic rats, respectively (P < 0.05). After 24 h of starvation, glucose production was not significantly different between control and cirrhotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
在喂食和禁食的四氯化碳（CCl4）诱导肝硬化大鼠中研究了能量代谢。在基础条件下（灌注液中不添加底物）以及用胰高血糖素（2 nM）和L-丙氨酸（20 mM）刺激后进行原位肝脏灌注实验。在基础条件下，无论代谢状态如何，肝硬化大鼠每克肝脏的耗氧量均降低。向灌注液中添加胰高血糖素/L-丙氨酸后，喂食和禁食的对照大鼠及肝硬化大鼠的耗氧量均显著增加。在基础条件下，肝硬化大鼠的葡萄糖生成减少了76%，对照肝脏和肝硬化肝脏分别平均为0.75±0.19与0.18±0.15 μmol·g肝脏-1·min-1（均值±标准误，P<0.05）。向灌注液中添加胰高血糖素/L-丙氨酸后，两组的葡萄糖生成均增加，与喂食的对照大鼠相比，喂食的肝硬化大鼠的葡萄糖生成减少了65%，对照大鼠和肝硬化大鼠分别平均为3.63±0.27与1.27±0.17 μmol·g肝脏-1·min-1（P<0.05）。刺激后的葡萄糖生成与氨基比林消除率常数分数（ABT-k）呈线性相关，ABT-k是体内肝功能的一项指标。禁食12小时后，与喂食状态相比，对照大鼠的刺激后葡萄糖生成减少了15%，喂食的肝硬化大鼠减少了65%，对照大鼠和肝硬化大鼠分别平均为3.07±0.22与0.33±0.03 μmol·g肝脏-1·min-1（P<0.05）。饥饿24小时后，对照大鼠和肝硬化大鼠的葡萄糖生成无显著差异。（摘要截选至250字）
