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Updated: May 24, 2026

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells (NPCs)
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Published on: March 2, 2018

Physiology of FGF15/19.

Stacey A Jones1

  • 1GlaxoSmithKline, Research Triangle Park, NC, USA. stacey.a.jones@gsk.com

Advances in Experimental Medicine and Biology
|March 8, 2012
PubMed
Summary

Mouse fibroblast growth factor 15 (Fgf15) and human fibroblast growth factor 19 (FGF19) are atypical FGF hormones. They regulate bile acid, gallbladder, and metabolic homeostasis via unique signaling pathways.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Research

Background:

  • Fibroblast growth factors (FGFs) typically regulate cell growth and differentiation.
  • Mouse Fgf15 and human FGF19 represent an atypical subfamily of FGFs functioning as endocrine hormones.
  • These FGFs exhibit distinct biochemical properties, including low heparin-binding affinity.

Purpose of the Study:

  • To review the diverse biological actions of mouse Fgf15 and human FGF19.
  • To elucidate the unique signaling mechanisms of this FGF subfamily.
  • To highlight their roles in enterohepatic signaling and metabolic regulation.

Main Methods:

  • Comparative sequence analysis of Fgf15 and FGF19.
  • Review of studies on FGF receptor signaling pathways.

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  • Analysis of Fgf15/FGF19 roles in enterohepatic circulation and metabolism.
  • Main Results:

    • Fgf15 and FGF19 are evolutionarily divergent but functionally conserved.
    • Their low heparin affinity allows for systemic circulation and distant signaling.
    • Signaling requires klotho cofactors, differing from typical FGF pathways.
    • They are crucial regulators of bile acid biosynthesis, gallbladder function, and metabolic homeostasis.

    Conclusions:

    • Mouse Fgf15 and human FGF19 are critical hormonal regulators in metabolic processes.
    • Their unique structure and signaling mechanisms enable systemic control of enterohepatic functions.
    • Further research into Fgf15/FGF19 pathways could offer therapeutic targets for metabolic disorders.