Leberhypertrophie und -atrophie im Pfortaderastligaturmodell der Ratte: Potentielle Rolle der Glukagon-Rezeptor-Expression
Liver hypertrophy and atrophy in rat portal branch ligation: potential role of glucagon-receptor expression
Background: Pre-operative portal branch ligation or embolization is a common procedure for the induction of contralateral liver hypertrophy in preparation of extended resections. Portal-derived hepatotrophic factors, e. g. gastrointestinal hormones like glucagon or insulin, are believed to be the basis of the phenomenon of volume-shifting. In this study, expression of glucagon-receptor-mRNA was examined in the rat model of 70% portal-branch ligation (PBL), 70% partial hepatectomy (HE) and sham operation (SO). Material and Methods: Two- to three-month-old male Wistar rats (200 g) were used. The animals were sacrified after 6, 12, 24, 48, 96, 192 h and 2 weeks. mRNA expression was assessed by RT-PCR and Northern hybridizations of total RNA using Digoxigenin-labeled DNA probes and chemoluminescent detection. The results of at least six animals per experiment and time point were analysed. Results: Following HE, glucagon-receptormRNA expression peaked with a maximum at 48 h after operation (median 1.6 fold vs. SO). In the PBL group, there was an analogous increase with a maximum at 48 h after operation (median 1.6 fold vs. SO). In the portal-ligated lobes, glucagon-receptor-mRNA expression was decreased compared to SO and PBL-non-ligated lobe. Albumin-mRNA was decreased 12 h after SO, HE and PBL in both lobes versus normal control liver tissue. In the ligated, shrinking lobe, albumin-mRNA expression was, after an initial decrease, intact during the observation. Conclusion: The increased expression of glucagonreceptor- mRNA correlates with the occurrence of liver regeneration after HE and the complex of hypertrophy-atrophy following PBL. This differential regulation of glucagonreceptor on the level of transcription might play a physiological role in liver regeneration and atrophy.
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