Portale Okklusion und Leberfunktion — Untersuchungen im Pfortaderastligaturmodell der Ratte

Abstract

Portal vein embolization has become a common method to prevent liver failure after extended hepatic resection. To date it is not known whether atrophy by portal deprivation with concomitant contralateral regeneration leads to alterations of liver function. On the basis of the rat model of portal branch ligation (PBL), this study focuses on the capacity to express genes coding for important determinants of liver function like glucose homeostasis and acute-phase response in comparison to partial hepatectomy (PH) and sham operation (SO) models. In regenerating liver tissue, a selective reduction of transcripts encoding glucose-6-phosphatase (G6P) during the prereplicative period was detected. In the portal-deprived liver tissue, the expression of liver function genes such as G6P or acute-phase reactants like fibronectin and C1-Inhibitor remained on the same level as observed after sham operation. The level of glycogen disappearance was lower after PBL in the regenerating lobe, compared to the residual liver after PR. Overall, portal deprived liver tissue after PBL retains its liver-specific differentiation and function and helps to maintain homeostasis, underlining the usefulness of this strategy in preventing posthepatectomy liver failure.