FGF19 as a Postprandial, Insulin-Independent Activator of Hepatic Protein and Glycogen Synthesis
Open accessAbstract
Fibroblast growth factor 19 regulates liver metabolism through a mechanism distinct from that of insulin.
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FGF19 induced ERK1/2 phosphorylation in mouse liver in vivo and in primary mouse and human hepatocytes in vitro.
“Consistent with previous reports29, FGF19 also induced phosphorylation at threonine-202 and tyrosine-204 of extracellular signal-regulated kinases ERK1 and ERK2 in the liver”
From Non-cell-autonomous activation of IL-6/STAT3 signaling mediates FGF19-driven hepatocarcinogenesis (2017) · cites this paper as [29]
The paper reports that FGF19 increased ERK1 and ERK2 phosphorylation in the livers of overnight-fasted mice (Fig. 1A), supporting the in vivo part of the claim. Its cell experiments report ERK phosphorylation in human HepG2 and rat HII4E tumor-derived cell lines (fig. S2A), not in primary mouse and human hepatocytes; the supplied copy also does not specify the ERK phosphorylation residues. No page number is provided for these passages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFGF19 increases liver protein and glycogen synthesis while repressing hepatic glucose production, independently from insulin.
“FGF19 also increases liver protein and glycogen synthesis while repressing hepatic glucose production 43, 44, in order to ensure proper postprandial energy storage independently from insulin.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [43]
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“, inhibition of gluconeogenesis, stimulation of glycogen synthesis (Kir et al., 2011; Potthoff et al., 2011).”
Background
- Authors
- Kir, S., Beddow, S. A., Samuel, V. T., Miller, P., Previs, S. F., Suino-Powell, K., Xu, H. E., Shulman, G. I., Kliewer, S. A., & Mangelsdorf, D. J.
- Affiliations
- Department of Pharmacology, University of Texas Southwestern Medical Center, 6001 Forest Park Road, Dallas, TX 75390, USA.
- Yale University (US)
- Case Western Reserve University (US)
- Van Andel Institute (US)
- Howard Hughes Medical Institute (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Kliewer, Steven A.
- Mangelsdorf, David J.
- ORCID
- Venue
- Science
- Published
- 2011-03-25
- Volume
- 331
- Issue
- 6024
- Pages
- 1621-1624
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3076083
- OpenAlex
- W1975673963
- Cited by
- 637
- References
- 27
- Citations by year
- 2026: 38 · 2025: 37 · 2024: 39 · 2023: 33 · 2022: 58 · 2021: 46 · 2020: 40 · 2019: 50 · 2018: 46 · 2017: 46 · 2016: 28 · 2015: 44 · 2014: 30 · 2013: 45 · 2012: 39
- FWCI
- 16.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DK67158, DK62434, DK40936, U24 DK076169)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- FGF19, FGF15, hepatic glycogen synthesis, hepatic protein synthesis, MAPK signaling, glycogen synthase, mRNA translation, lipogenesis, glucose homeostasis, diabetes mellitus
- MeSH terms
- Animals, Blood Glucose, Diabetes Mellitus, Experimental, Fibroblast Growth Factors, Glucose, Glycogen Synthase, Humans, Insulin, Liver, Liver Glycogen, Male, Mice, Inbred C57BL, Phosphorylation, Protein Biosynthesis, Signal Transduction, MAP Kinase Signaling System, Glycogen Synthase Kinase 3, Ribosomal Protein S6, Eukaryotic Initiation Factors, Proto-Oncogene Proteins c-akt, Mice, Hep G2 Cells
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