Z Gastroenterol 2015; 53 - A3_25
DOI: 10.1055/s-0034-1397146

Representation of human non-alcoholic fatty liver disease in murine models

A Teufel 1, T Itzel 1, W Erhart 2, M Brosch 3, YO Kim 4, W von Schönfels 5, A Herrmann 2, S Brückner 3, F Stickel 6, T Chavakis 7, C Hellerbrand 1, T Becker 5, S Schreiber 2, D Schuppan 4, C Schafmeier 5, J Hampe 1
  • 1University of Regensburg, Department of Medicine I, Regensburg, Germany
  • 2University of Kiel, Department of Internal Medicine I, Kiel, Germany
  • 3Technical Unversity Dresden, Medical Department I, Dresden, Germany
  • 4University of Mainz, Department of Medicine I, Mainz, Germany
  • 5University of Kiel, Department Visceral and Thoracic Surgery, Kiel, Germany
  • 6University of Berne, Department of Clinical Research, Berne, Switzerland
  • 7Technical University Dresden, Department of Pathobiochemistry, Dresden, Germany

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in industrialized countries. Murine models are the key mechanistic platform for the disease. We systematically evaluated genome-wide mRNA expression data from five commonly used murine models of NAFLD (high-fat diet, MCD diet, streptozotocin diet, PTEN (Fox) KO) in comparison to human data from 39 controls and 77 NAFLD samples spanning the range of the phenotype. First, profound differences between human and murine expression patterns exist, that override any disease or phenotype signature. In fact, from the significantly regulated human genes in NASH/NAFLD only between 1 and 16 are significantly and concordantly regulated in mice. The dataset, depending on mouse model and human phenotype, shows correct reflection of key pathways, lack of regulation, or reverse effects thereby providing a guide for murine model selection in future experiments to improve applicability to human NAFLD.

Corresponding author: Teufel, Andreas

E-Mail: andreas.teufel@ukr.de