Evidence map›Paper›PMID 28178326›Full record

ArticlePloS one2017

Quantitative liver proteomics identifies FGF19 targets that couple metabolism and proliferation.

Vittoria Massafra, Alexandra Milona, Harmjan R Vos, Boudewijn M T Burgering, Saskia W C van Mil

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Intestinal farnesoid X receptor signaling controls hepatic fatty acid oxidation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  14. Review: Pathogenesis of cholestatic liver diseases.World journal of hepatology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Vittoria MassafraCenter for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Alexandra MilonaCenter for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Harmjan R VosCenter for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Boudewijn M T BurgeringCenter for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Saskia W C van MilCenter for Molecular Medicine, UMC Utrecht, Utrecht, The Netherlands.
Utrecht University · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 19 (FGF19) is a gut-derived peptide hormone that is produced following activation of Farnesoid X Receptor (FXR). FGF19 is secreted and signals to the liver, where it contributes to the homeostasis of bile acid (BA), lipid and carbohydrate metabolism. FGF19 is a promising therapeutic target for the metabolic syndrome and cholestatic diseases, but enthusiasm for its use has been tempered by FGF19-mediated induction of proliferation and hepatocellular carcinoma. To inform future rational design of FGF19-variants, we have conducted temporal quantitative proteomic and gene expression analyses to identify FGF19-targets related to metabolism and proliferation. Mice were fasted for 16 hours, and injected with human FGF19 (1 mg/kg body weight) or vehicle. Liver protein extracts (containing "light" lysine) were mixed 1:1 with a spike-in protein extract from 13C6-lysine metabolically labelled mouse liver (containing "heavy" lysine) and analysed by LC-MS/MS. Our analyses provide a resource of FGF19 target proteins in the liver. 189 proteins were upregulated (≥ 1.5 folds) and 73 proteins were downregulated (≤ -1.5 folds) by FGF19. FGF19 treatment decreased the expression of proteins involved in fatty acid (FA) synthesis, i.e., Fabp5, Scd1, and Acsl3 and increased the expression of Acox1, involved in FA oxidation. As expected, FGF19 increased the expression of proteins known to drive proliferation (i.e., Tgfbi, Vcam1, Anxa2 and Hdlbp). Importantly, many of the FGF19 targets (i.e., Pdk4, Apoa4, Fas and Stat3) have a dual function in both metabolism and cell proliferation. Therefore, our findings challenge the development of FGF19-variants that fully uncouple metabolic benefit from mitogenic potential.

Indexed as

Energy MetabolismProteomeProteomicsAnimalsCell ProliferationCell SurvivalCell Transformation, NeoplasticFibroblast Growth FactorsGene ExpressionHumansLiverMaleMiceRecombinant ProteinsRNA, MessengerFGF19 protein, humanFibroblast Growth FactorsProteomeRecombinant ProteinsRNA, Messenger

Identifiers

PMID28178326
PMCPMC5298232
OpenAlexW2586706028

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.