Rich-Denson C, Kimura R E
Department of Pediatrics, University of Utah School of Medicine, Salt Lake City 841322.
Biochem J. 1988 Sep 15;254(3):931-4. doi: 10.1042/bj2540931.
Studies in vitro and acute studies in vivo have indicated that the intestine may be a significant producer of portal-venous lactate, a major carbon source for liver glycogen synthesis. To determine if a significant portion of intraluminal glucose is converted into lactate by the intestine in vivo, we measured the ratio of intraluminal glucose which is absorbed intact into the portal vein to that which is converted into lactate by the intestine in a chronically catheterized rat, in which catheters were surgically placed into the portal vein, aorta and stomach. This ratio was 36-42 when intraluminal [U-14C]glucose concentrations of 5-200 mM were used, suggesting that the intestine may not be a significant source of portal-venous lactate in vivo. Under hypoxic conditions [PaO2 less than 40 Torr (5.3 kPa)] the ratio decreased to 2.1, indicating that the amount of intraluminal glucose converted into lactate had increased significantly.
体外研究和体内急性研究表明,肠道可能是门静脉乳酸的重要产生部位,而门静脉乳酸是肝脏糖原合成的主要碳源。为了确定管腔内葡萄糖在体内是否有很大一部分被肠道转化为乳酸,我们在一只长期插管的大鼠中测量了完整吸收进入门静脉的管腔内葡萄糖与被肠道转化为乳酸的管腔内葡萄糖的比例,该大鼠通过手术将导管分别置于门静脉、主动脉和胃中。当管腔内[U-14C]葡萄糖浓度为5-200 mM时,该比例为36-42,这表明在体内肠道可能不是门静脉乳酸的重要来源。在低氧条件下[动脉血氧分压小于40 Torr(5.3 kPa)],该比例降至2.1,表明管腔内转化为乳酸的葡萄糖量显著增加。