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Gut 63:205-206 doi:10.1136/gutjnl-2013-305227
  • PostScript
  • Letter

Observations suggesting bioactive Fgf15 is not present in mouse blood

Open Access
  1. Mats Rudling
  1. Correspondence to Professor Mats Rudling, Metabolism Unit, Center for Endocrinology, Metabolism, and Diabetes, Karolinska Institute, C2-94, Karolinska University Hospital Huddinge, Stockholm S-141 86, Sweden; mats.rudling{at}ki.se
  • Received 5 May 2013
  • Revised 7 May 2013
  • Accepted 8 May 2013
  • Published Online First 8 June 2013

I read with interest the paper by Uriarte et al,1 in which the authors conclude that ‘Fgf15 is a key mediator of the liver growth-promoting effects of bile acids.’

There are reasons to question the conclusions drawn in this paper. Due to space limit I forward three issues.

(1) Fgf15 exerts its effects via FGFR4 as mentioned. The authors have not recognised a report by Yu et al 2 showing that deletion of FGFR4 does not alter the ability of the liver to regenerate after partial hepatectomy.

How can …

Open Access


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