Perturbation of acyl ghrelin profile after liver transplantation.

BACKGROUND: A significant problem to be solved for patients after liver transplantation (LT) is malnutrition with anorexia in the early posttransplant period. We hypothesized that this problem was due to the change in ghrelin metabolism during LT. The aim of this study was to examine the balance of acyl ghrelin (AG) and desacyl ghrelin and the dependence of the regulation mechanism on hepatic-related enzymes in patients during LT.

MATERIALS AND METHODS: AG, desacyl ghrelin, and acyl/total ghrelin (A/T) concentrations in blood samples were measured in 15 patients with liver failure (LF), 15 patients after LT, and 10 controls. The correlations between the participants' ghrelin profiles and hepatic function-related data, including liver enzymes, were evaluated. In vitro assays using synthetic AG for assessment of deacylation activity in serum were performed.

RESULTS: AG and A/T ratio were significantly higher in the LF patients than the patients after LT and controls (AG: 25.9 ± 12.6 versus 16.4 ± 12.6 and 9.8 ± 7.6 fmol/mL, P < 0.05; A/T ratio: 17.4 ± 4.1 versus 12.2 ± 5.5 and 11.8% ± 5.9%, P < 0.05). The serum cholinesterase level was inversely correlated with AG and A/T ratio (P < 0.01). In vitro assays showed that deacylation activity was significantly lower in patients with LF than controls (10.5% versus 42.4%, 90 min; P < 0.01). Degradation of AG was partially suppressed by a cholinesterase inhibitor.

CONCLUSIONS: Deacylation activity was lower in LF patients, which could cause elevation of AG levels. Serum cholinesterase may be responsible for deacylation in humans.