Cited by 150Fibroblast Growth Factor ResearchAlcohol Consumption and Health EffectsLiver physiology and pathology

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Fibroblast growth factor 21 (FGF21) is robustly induced by ethanol and has a protective role in ethanol associated liver injury

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Desai, Bhavna N., Singhal, Garima, Watanabe, Mikiko, Stevanovic, Darko, Lundasen, Thomas, Fisher, ffolliott M., Mather, Marie L., Vardeh, Hilde G., Douris, Nicholas, Adams, Andrew C., Nasser, Imad A., FitzGerald, Garret A., Flier, Jeffrey S., Skarke, Carsten, Maratos-Flier, Eleftheria·2017·Molecular Metabolism

DOI 10.1016/j.molmet.2017.08.004PMC PMC5681240

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Abstract

OBJECTIVE: Excess ethanol consumption has serious pathologic consequences. In humans, repeated episodes of binge drinking can lead to liver damage and have adverse effects on other organs such as pancreas and brain. Long term chronic consumption of ethanol can also result in progressive alcoholic liver disease and cirrhosis. Fibroblast growth factor 21 (FGF21) is a metabolic regulator with multiple physiologic functions. FGF21 is a novel biomarker for non-alcoholic fatty liver disease (NAFLD) in humans and limits hepatotoxicity in mice. Therefore, we explored the possibility that FGF21 plays a role in response to ethanol consumption in both humans and mice. METHODS: We used a binge drinking paradigm in humans to examine the effect of acute ethanol consumption on circulating FGF21. We adapted this paradigm to evaluate the acute response to ethanol in mice. We then examined the role of FGF21 on liver pathology in two models of chronic ethanol consumption in both wild type (WT) mice and mice lacking FGF21 (FGF21-KO). RESULTS: Acute ethanol consumption resulted in a robust induction of serum FGF21 after 6 h in both humans and mice. Serum ethanol peaked at 1 h in both species and was cleared by 6 h. Ethanol clearance was the same in WT and FGF21-KO mice, indicating that FGF21 does not play a major role in ethanol metabolism in a binge paradigm. When FGF21-KO mice were fed the Lieber-DeCarli diet, a high fat diet supplemented with ethanol, a higher mortality was observed compared to WT mice after 16 days on the diet. When FGF21-KO mice consumed 30% ethanol in drinking water, along with a normal chow diet, there was no mortality observed even after 16 weeks, but the FGF21-KO mice had significant liver pathology compared to WT mice. CONCLUSIONS: Acute or binge ethanol consumption significantly increases circulating FGF21 levels in both humans and mice. However, FGF21 does not play a role in acute ethanol clearance. In contrast, chronic ethanol consumption in the absence of FGF21 is associated with significant liver pathology alone or in combination with excess mortality, depending on the type of diet consumed with ethanol. This suggests that FGF21 protects against long term ethanol induced hepatic damage and may attenuate progression of alcoholic liver disease. Further study is required to assess the therapeutic potential of FGF21 in the treatment of alcoholic liver disease.

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Authors: Desai, B. N., Singhal, G., Watanabe, M., Stevanovic, D., Lundasen, T., Fisher, F. M., Mather, M. L., Vardeh, H. G., Douris, N., Adams, A. C., Nasser, I. A., FitzGerald, G. A., Flier, J. S., Skarke, C., & Maratos-Flier, E.
Affiliations: Beth Israel Deaconess Medical Center (US)
Eli Lilly (United States) (US)
University of Pennsylvania (US)
ORCID: Watanabe, Mikiko
Mather, Marie L.
Douris, Nicholas
Adams, Andrew C.
Nasser, Imad A.
FitzGerald, Garret A.
Flier, Jeffrey S.
Skarke, Carsten
Venue: Molecular Metabolism
Publisher: Elsevier BV
Published: 2017-11
Volume: 6
Issue: 11
Pages: 1395-1406
ISSN: 2212-8778 (ISSN-L)
DOI: 10.1016/j.molmet.2017.08.004
PMC: PMC5681240
OpenAlex: W2749688538
Cited by: 150
References: 43
Citations by year: 2026: 12 · 2025: 20 · 2024: 17 · 2023: 16 · 2022: 19 · 2021: 21 · 2020: 17 · 2019: 15 · 2018: 12
FWCI: 4.92
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor)
Locations: Molecular Metabolism (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
Funders: American Heart Association
JPB Foundation
National Institutes of Health (UL1TR000003, DK028082, DK034854, ES013508)
Harvard Digestive Diseases Center, Harvard University (P30DK034854, DK034854)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK P30, DK034854, DK028082, R01DK028082, P30DK034854)
National Institute of Environmental Health Sciences (ES013508-05, ES013508, P30ES013508)
National Center for Research Resources (UL1RR024134)
National Center for Advancing Translational Sciences
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: FGF21, ethanol, binge drinking, alcoholic liver disease, ethanol-induced liver injury, hepatoprotection, FGF21 knockout mice, ethanol clearance, mortality, biomarkers, chronic alcohol consumption, Lieber-DeCarli diet, alcohol metabolism, liver pathology
MeSH terms: Adult, Ethanol, Animals, Fatty Liver, Alcoholic, Female, Fibroblast Growth Factors, Humans, Liver, Liver Cirrhosis, Liver Diseases, Alcoholic, Longitudinal Studies, Male, Mice, Inbred C57BL, Random Allocation, Mice, Knockout, Mice

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Fibroblast growth factor 21 (FGF21) is robustly induced by ethanol and has a protective role in ethanol associated liver injury

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