Langhans W
Institute of Veterinary Physiology, University of Zurich, Switzerland.
Physiol Behav. 1991 Jun;49(6):1203-9. doi: 10.1016/0031-9384(91)90352-o.
Changes in hepatic vein, hepatic portal vein and aortal plasma levels of glucose, lactate, nonesterified fatty acids, and D-3-hydroxybutyrate as well as changes in hepatic glycogen and lactate levels were studied during feeding after 12 h of food deprivation in rats. Feeding caused an increase in portal vein lactate concentration and a transient net hepatic lactate uptake that led to hepatic lactate accumulation. As in previous experiments, feeding was associated with hepatic glycogenolysis and net hepatic glucose release, despite a profound increase in portal vein plasma glucose. Net hepatic uptake of nonesterified fatty acids and net hepatic release of D-3-hydroxybutyrate declined during feeding but did not cease, suggesting that hepatic fatty acid oxidation continued throughout feeding. A prandial net intestinal uptake from arterial blood was observed for nonesterified fatty acids and D-3-hydroxybutyrate, while a net intestinal release was found for glucose and lactate. The results are consistent with the idea that under the conditions tested, glucose, lactate and nonesterified fatty acids jointly activate a hepatic metabolic mechanism of satiety.
在大鼠禁食12小时后进食期间,研究了肝静脉、肝门静脉和主动脉血浆中葡萄糖、乳酸、非酯化脂肪酸和D-3-羟基丁酸水平的变化,以及肝糖原和乳酸水平的变化。进食导致门静脉乳酸浓度升高和短暂的肝脏乳酸净摄取,进而导致肝脏乳酸积累。与之前的实验一样,尽管门静脉血浆葡萄糖大幅增加,但进食仍与肝糖原分解和肝脏葡萄糖净释放有关。进食期间,肝脏对非酯化脂肪酸的净摄取和D-3-羟基丁酸的肝脏净释放下降,但并未停止,这表明在整个进食过程中肝脏脂肪酸氧化仍在继续。观察到非酯化脂肪酸和D-3-羟基丁酸有餐后从动脉血的净肠道摄取,而葡萄糖和乳酸则有净肠道释放。结果与以下观点一致,即在测试条件下,葡萄糖、乳酸和非酯化脂肪酸共同激活肝脏的饱腹感代谢机制。