Niewoehner C B, Nuttall F Q
Endocrinology, Metabolism, and Nutrition Section, Veterans Administration Medical Center, Minneapolis 55417.
Am J Physiol. 1989 Jun;256(6 Pt 1):E811-7. doi: 10.1152/ajpendo.1989.256.6.E811.
Current evidence suggests that, during the transition from the fasted to the fed state, liver glycogen is synthesized primarily from gluconeogenic precursors rather than from glucose unless the circulating glucose concentration is high. In the fed state the glucose concentration already is elevated. We aimed to determine whether administration of an additional oral glucose load (4 g/kg) to chow- or high-carbohydrate diet-adapted (CHO) rats would further increase the glucose concentration and result in increased direct glucose uptake. In the chow- and CHO-fed rats, 70 and 98% of the administered glucose was absorbed by 120 min. In the chow-fed rats the glucose concentration entering the liver increased by only 1.0 mM from 8.0 to 9.0 mM; no net hepatic glucose uptake was observed. In the CHO-adapted rats the entering glucose concentration increased transiently by 3.5 mM from 8.0 to 11.5 mM. This was associated with net glucose uptake, which continued until the entering glucose concentration fell below 9.5 mM, the entering glucose concentration threshold above which net glucose uptake was observed previously in fasted rats. Net hepatic glucose uptake could not be correlated with insulin or hepatic intracellular glucose concentrations. Net glycogen synthesis did not occur in either group. We could not account for the absorbed glucose by the rise in portal glucose concentrations or by increased muscle glycogen deposition. The fate of much of the absorbed glucose remains unknown.
目前的证据表明,在从禁食状态转变为进食状态的过程中,肝脏糖原主要由糖异生前体合成,而非由葡萄糖合成,除非循环葡萄糖浓度很高。在进食状态下,葡萄糖浓度已经升高。我们旨在确定,给食用普通饲料或高碳水化合物饮食(CHO)的大鼠额外口服葡萄糖负荷(4 g/kg)是否会进一步提高葡萄糖浓度,并导致直接葡萄糖摄取增加。在食用普通饲料和CHO的大鼠中,给药的葡萄糖在120分钟内分别有70%和98%被吸收。在食用普通饲料的大鼠中,进入肝脏的葡萄糖浓度仅从8.0 mM增加到9.0 mM,增加了1.0 mM;未观察到肝脏净葡萄糖摄取。在适应CHO的大鼠中,进入的葡萄糖浓度从8.0 mM短暂增加到11.5 mM,增加了3.5 mM。这与净葡萄糖摄取有关,净葡萄糖摄取一直持续到进入的葡萄糖浓度降至9.5 mM以下,该进入葡萄糖浓度阈值是之前在禁食大鼠中观察到有净葡萄糖摄取时的阈值。肝脏净葡萄糖摄取与胰岛素或肝脏细胞内葡萄糖浓度无关。两组均未发生净糖原合成。我们无法通过门静脉葡萄糖浓度的升高或肌肉糖原沉积的增加来解释吸收的葡萄糖去向。大部分吸收的葡萄糖的去向仍然未知。