Hamberg O, Almdal T P
Department of Medicine A-2101, Rigshospitalet, Copenhagen, Denmark.
JPEN J Parenter Enteral Nutr. 1996 Mar-Apr;20(2):139-44. doi: 10.1177/0148607196020002139.
Xylitol exerts a nitrogen-sparing effect in stress catabolic states with hyperglucagonemia, but the mechanism(s) is unknown. We examined the effects of xylitol on urea synthesis during physiologic glucagon concentrations and during hyperglucagonemia.
Urea synthesis was measured independently of blood amino acid concentration by means of functional hepatic nitrogen clearance (FHNC) (ie, the linear slope of the relation between urea synthesis rate and blood alpha-amino nitrogen concentration during infusion of alanine). FHNC was measured on four separate occasions in each of seven healthy subjects: during constant infusion of alanine alone, alanine superimposed on a constant infusion of xylitol (blood xylitol 1 mmol/L), alanine superimposed on infusion of glucagon, and alanine superimposed on infusions of xylitol and glucagon.
During alanine infusion alone, plasma glucagon rose to -170 ng/L, and FHNC was (mean +/- sem) 27.9 +/- 1.3 L/h. Xylitol did not affect plasma glucagon and only moderately reduced FHNC to 24.3 +/- 1.0 L/h (p < .05). Glucagon infusion increased plasma glucagon to -450 ng/L and FHNC twofold to 50.9 +/- 6.2 L/h; this increase was totally prevented by the addition of xylitol that reduced FHNC to 27.4 +/- 2.6 L/h (p < .01).
The results show that xylitol only inhibited FHNC minimally during spontaneous glucagon levels. In contrast, xylitol completely inhibits the increase in FHNC by glucagon. This suggests that the mechanism whereby xylitol reduces nitrogen loss in stress catabolic conditions with hyperglucagonemia involves an effect on liver metabolism. The mechanism is unknown but may be related to depletion of hepatocyte adenine nucleotides.
木糖醇在胰高血糖素血症的应激分解代谢状态下具有氮节约作用，但其机制尚不清楚。我们研究了木糖醇在生理胰高血糖素浓度和高胰高血糖素血症期间对尿素合成的影响。
通过功能性肝氮清除率（FHNC）（即输注丙氨酸期间尿素合成速率与血α-氨基氮浓度之间关系的线性斜率）独立于血氨基酸浓度测量尿素合成。在7名健康受试者中，每人在四个不同时间测量FHNC：单独持续输注丙氨酸期间、丙氨酸叠加在持续输注木糖醇（血木糖醇1 mmol/L）期间、丙氨酸叠加在输注胰高血糖素期间以及丙氨酸叠加在输注木糖醇和胰高血糖素期间。
单独输注丙氨酸期间，血浆胰高血糖素升至-170 ng/L，FHNC为（均值±标准误）27.9±1.3 L/h。木糖醇不影响血浆胰高血糖素，仅适度降低FHNC至24.3±1.0 L/h（p<0.05）。输注胰高血糖素使血浆胰高血糖素升至-450 ng/L，FHNC增加两倍至50.9±6.2 L/h；添加木糖醇将FHNC降至27.4±2.6 L/h（p<0.01）可完全阻止这种增加。
结果表明，在自发胰高血糖素水平期间，木糖醇仅轻微抑制FHNC。相比之下，木糖醇完全抑制胰高血糖素引起的FHNC增加。这表明木糖醇在胰高血糖素血症的应激分解代谢条件下减少氮损失的机制涉及对肝脏代谢的影响。其机制尚不清楚，但可能与肝细胞腺嘌呤核苷酸耗竭有关。
