EFFECTS OF XYLITOL ON UREA SYNTHESIS IN PATIENTS WITH CIRRHOSIS OF THE LIVER

Background: In individuals with cirrhosis the normal inhibiting effect of glucose on urea synthesis is lost, probably because of very high c oncentrations of glucagon. In agreement, glucose does not prevent the inducing effect of glucagon on urea synthesis in normal humans. In con trast, the sugar alcohol, xylitol, prevents the increasing effect of g lucagon in normal humans. We, therefore, examined the effect of xylito l on urea synthesis in individuals with cirrhosis and hyperglucagonemi a. Methods: Urea synthesis, calculated as urinary excretion rate corre cted for accumulation in total body water and intestinal loss, was mea sured during infusion of alanine (2 mmol/[h.kg body wt]) and during in fusion of alanine superimposed on infusion of xylitol (0.12 g/[h.kg bo dy wt]) in 8 individuals with biopsy-proven alcoholic cirrhosis. The f unctional hepatic nitrogen clearance (FHNC), ie, urea synthesis expres sed independent of changes in plasma amino acid concentration, was cal culated as the slope of the Linear relation between the urea synthesis rate and the plasma amino acid concentration. Results: All individual s had elevated basal plasma glucagon concentration (261 +/- 61 ng/L; m ean +/- SEM) and a markedly increased response to alanine infusion (10 37 +/- 226 ng/L). This was not changed by xylitol. Neither the basal u rea synthesis rate (13.2 +/- 2.5 mmol/h) nor the alanine-stimulated ur ea 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). C onclusions: Xylitol reduces neither urea synthesis nor FHNC. The data do not support an important role of xylitol as a nitrogen-sparing agen t in cirrhosis.