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Observations suggesting bioactive Fgf15 is not present in mouse blood
  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}

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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 …

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