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Main research

The farnesoid X receptor (FXR) is a nuclear transcription factor that is activated by bile acids and feedback-regulates bile acid and lipid metabolism. Extensive research over the past decade has placed specific FXR activation at the center of promising novel treatment options for cholestatic liver disorders and metabolic diseases such as type 2 diabetes, atherosclerosis and, in particular, non-alcoholic steatohepatitis.

To date, FXR activation studies have been conducted in animal models of cholestatic and fatty liver diseases and only subsequently translated into models of human relevance, mainly ex vivo/in vitro human cell systems. However, this strategy might miss important mechanistic insights since bile acid species (i.e. potential FXR ligands) differ profoundly between humans and mice. Moreover, bile acids activate several other FXR-independent metabolic signaling pathways and some might even act as FXR antagonists. Furthermore, the gut microbiota regulates species-specific secondary bile acid metabolism. Thus, changes in FXR-activated feedback loops might be differently translated between humans and rodents and depend on specific gut microbiota.

We aim to improve the translation of animal model studies on FXR activation to human diseases by identifying specific differences in FXR-dependent regulatory pathways between mice and humans and by comparing global DNA binding sites of FXR in mouse and human liver genomes. Our ultimate goal is to develop new treatment options for human cholestatic and fatty liver diseases.


Contact Information

Hanns-Ulrich Marschall

Wallenberg Laboratory, SU/Sahlgrenska, SE-413 45 Göteborg, Sweden

Visiting Address:
Bruna Stråket 16

+46 (0)70-8774073

Page Manager: Anna Hallén|Last update: 8/27/2012

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