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. 2018 Nov 21;8:17210. doi: 10.1038/s41598-018-35496-z

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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M52 is a non-tumorigenic variant of FGF19 that retains activity in regulating BA synthesis. (a) Alignment of protein sequences of M52 and FGF19 in the N-terminal region. Mutations introduced into M52 are underlined. (b) Repression of CYP7A1 mRNA expression by AAV-M52 vs AAV-GFP in primary human hepatocytes. (c) Plasma levels of transgene expression, (d) number of tumors per liver, (e) liver weight and (f) percentage of liver weight over body weight ratio in db/db mice injected with AAV-GFP (black bar), AAV-FGF19 (red bar) or AAV-FGF19-M52 (blue bar). All values represent means ± SEM. Statistical significance comparing either FGF19 or M52 versus control (*p < 0.05, **p < 0.01, ***p < 0.001) assessed by one-way ANOVA followed by Dunnett’s post hoc test.