木糖醇对肝硬化患者尿素合成的影响。

Effects of xylitol on urea synthesis in patients with cirrhosis of the liver.

作者信息

Pedersen E, Hamberg O, Borg B, Haaber A, Enemark H, Vilstrup H

机构信息

Department of Medicine F, Glostrup University Hospital, Copenhagen, Denmark.

出版信息

JPEN J Parenter Enteral Nutr. 1998 Sep-Oct;22(5):320-5. doi: 10.1177/0148607198022005320.

DOI:10.1177/0148607198022005320

PMID:9739037

Abstract

BACKGROUND

In individuals with cirrhosis the normal inhibiting effect of glucose on urea synthesis is lost, probably because of very high concentrations of glucagon. In agreement, glucose does not prevent the inducing effect of glucagon on urea synthesis in normal humans. In contrast, the sugar alcohol, xylitol, prevents the increasing effect of glucagon in normal humans. We, therefore, examined the effect of xylitol on urea synthesis in individuals with cirrhosis and hyperglucagonemia.

METHODS

Urea synthesis, calculated as urinary excretion rate corrected for accumulation in total body water and intestinal loss, was measured during infusion of alanine (2 mmol/[h x kg body wt]) and during infusion of alanine superimposed on infusion of xylitol (0.12 g/[h x kg body wt]) in 8 individuals with biopsy-proven alcoholic cirrhosis. The functional hepatic nitrogen clearance (FHNC), ie, urea synthesis expressed independent of changes in plasma amino acid concentration, was calculated as the slope of the linear relation between the urea synthesis rate and the plasma amino acid concentration.

RESULTS

All individuals had elevated basal plasma glucagon concentration (261 +/- 61 ng/L; mean +/- SEM) and a markedly increased response to alanine infusion (1037 +/- 226 ng/L). This was not changed by xylitol. Neither the basal urea synthesis rate (13.2 +/- 2.5 mmol/h) nor the alanine-stimulated urea synthesis rate (76.8 +/- 3.64 mmol/h) was changed by xylitol. FHNC during the infusion of alanine alone was 10.5 +/- 0.9 L/h and did not change during the concomitant infusion of xylitol (10.1 +/- 1.1 L/h).

CONCLUSIONS

Xylitol reduces neither urea synthesis nor FHNC. The data do not support an important role of xylitol as a nitrogen-sparing agent in cirrhosis.

摘要

背景

在肝硬化患者中，葡萄糖对尿素合成的正常抑制作用丧失，可能是由于胰高血糖素浓度极高。同样，葡萄糖并不能阻止胰高血糖素对正常人尿素合成的诱导作用。相比之下，糖醇木糖醇可阻止胰高血糖素对正常人的增强作用。因此，我们研究了木糖醇对肝硬化和高胰高血糖素血症患者尿素合成的影响。

方法

在8例经活检证实为酒精性肝硬化的患者中，在输注丙氨酸（2 mmol/[h×kg体重]）期间以及在输注丙氨酸的同时叠加输注木糖醇（0.12 g/[h×kg体重]）期间，测量尿素合成，计算方法为尿排泄率经全身水蓄积和肠道丢失校正后得出。计算功能性肝氮清除率（FHNC），即独立于血浆氨基酸浓度变化表示的尿素合成，计算方法为尿素合成率与血浆氨基酸浓度之间线性关系的斜率。

结果

所有患者基础血浆胰高血糖素浓度均升高（261±61 ng/L；平均值±标准误），对丙氨酸输注的反应明显增强（1037±226 ng/L）。木糖醇对此无改变。木糖醇既未改变基础尿素合成率（13.2±2.5 mmol/h），也未改变丙氨酸刺激后的尿素合成率（76.8±3.64 mmol/h）。单独输注丙氨酸期间的FHNC为10.5±0.9 L/h，在同时输注木糖醇期间未改变（10.1±1.1 L/h）。