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Sci Rep. 2018 Nov 15;8(1):16858. doi: 10.1038/s41598-018-35325-3.

Liver-specific Repin1 deficiency impairs transient hepatic steatosis in liver regeneration.

Author information

1
Institute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany. kerstin.abshagen@uni-rostock.de.
2
Institute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
3
QIMR Berghofer Medical Research Institute, 200 Herston Road, Herston, QLD, 4006, Australia.
4
Silence Therapeutics GmbH, Berlin, Robert Rössle Strasse 10, 13125, Berlin, Germany.
5
Department of Medicine, University of Leipzig, Liebigstrasse 18, 04103, Leipzig, Germany.
6
Dr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Auerbachstrasse 112, 70376 Stuttgart and University of Tuebingen, Tuebingen, Germany.
7
Medical Biology and Electron Microscopy Centre, University Medicine Rostock, Strempelstrasse 14, 18057, Rostock, Germany.
8
Integrated Research and Treatment Center (IFB) Adiposity Diseases, University of Leipzig, Liebigstrasse 19-21, 04103, Leipzig, Germany.

Abstract

Transient hepatic steatosis upon liver resection supposes functional relationships between lipid metabolism and liver regeneration. Repin1 has been suggested as candidate gene for obesity and dyslipidemia by regulating key genes of lipid metabolism and lipid storage. Herein, we characterized the regenerative potential of mice with a hepatic deletion of Repin1 (LRep1-/-) after partial hepatectomy (PH) in order to determine the functional significance of Repin1 in liver regeneration. Lipid dynamics and the regenerative response were analyzed at various time points after PH. Hepatic Repin1 deficiency causes a significantly decreased transient hepatic lipid accumulation. Defects in lipid uptake, as analyzed by decreased expression of the fatty acid transporter Cd36 and Fatp5, may contribute to attenuated and shifted lipid accumulation, accompanied by altered extent and chronological sequence of liver cell proliferation in LRep1-/- mice. In vitro steatosis experiments with primary hepatocytes also revealed attenuated lipid accumulation and occurrence of smaller lipid droplets in Repin1-deficient cells, while no direct effect on proliferation in HepG2 cells was observed. Based on these results, we propose that hepatocellular Repin1 might be of functional significance for early accumulation of lipids in hepatocytes after PH, facilitating efficient progression of liver regeneration.

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