Research ArticleImpaired liver regeneration of steatotic rats after portal vein ligation: A particular emphasis on 99mTc-DISIDA scintigraphy and adiponectin signaling

Background & AimsPortal vein ligation (PVL) is increasingly employed prior to major hepatectomy in order to enhance the volume of the future liver remnant (FLR) and to avoid post-hepatectomy liver failure. The efficacy of PVL on subjects with non-alcohol fatty liver disease (NAFLD) is largely unknown.MethodsSprague-Dawley rats fed with normal diet (control) and methionine-choline deficient diet (MCD) were used. The animals underwent PVL and were sacrificed at indicated time points.ResultsLivers from MCD rats exhibited a decreased BrdU and Ki-67 labelling index, and an increased apoptotic index after PVL compared to normal rats; as a net effect, MCD rats exhibited a decrease in their restituted liver mass and redistributed volume ratio, compared to normal rats. Normal rats displayed similar serum levels of ICG15-R before and after PVL; whereas MCD rats displayed reduced ICG15-R after PVL. Using 99mTc-DISIDA scintigraphy examination, livers from MCD rats exhibited decreased HEF and prolonged TE1/2 of FLR after PVL, indicating deteriorating hepatocyte function despite the shift in volume. The basal level of plasma TNFα, IL-1α, IL-1β, and IL-10 of MCD rats was significantly increased before PVL compared to normal rats; however their plasma level did not increase in response to PVL as in normal rats. Hepatic adiponectin mRNA surged in MCD rats after PVL, whereas its receptors, AdipoR1 and AdipoR2, were paradoxically down-regulated. PPARα, a down-stream molecule of AdipoR2 axis, was also decreased in MCD rats.ConclusionsReduced regenerated liver mass and deteriorated hepatocyte function of the FLR from steatotic rats after PVL may be associated with deranged Kupffer cell-mediated cytokine expression and disrupted adiponectin signalling.