Fibroblast growth factor 21 is elevated in metabolically unhealthy obesity and affects lipid deposition, adipogenesis, and adipokine secretion of human abdominal subcutaneous adipocytes
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OBJECTIVE: Serum concentrations of the hepatokine fibroblast growth factor (FGF) 21 are elevated in obesity, type-2 diabetes, and the metabolic syndrome. We asked whether FGF21 levels differ between subjects with metabolically healthy vs. unhealthy obesity (MHO vs. MUHO), opening the possibility that FGF21 is a cross-talker between liver and adipose tissue in MUHO. Furthermore, we studied the effects of chronic FGF21 treatment on adipocyte differentiation, lipid storage, and adipokine secretion. METHODS: In 20 morbidly obese donors of abdominal subcutaneous fat biopsies discordant for their whole-body insulin sensitivity (hereby classified as MHO or MUHO subjects), serum FGF21 was quantified. The impact of chronic FGF21 treatment on differentiation, lipid accumulation, and adipokine release was assessed in isolated preadipocytes differentiated in vitro. RESULTS: Serum FGF21 concentrations were more than two-fold higher in MUHO as compared to MHO subjects (457 ± 378 vs. 211 ± 123 pg/mL; p < 0.05). FGF21 treatment of human preadipocytes for the entire differentiation period was modestly lipogenic (+15%; p < 0.05), reduced the expression of key adipogenic transcription factors (PPARG and CEBPA, -15% and -40%, respectively; p < 0.01 both), reduced adiponectin expression (-20%; p < 0.05), markedly reduced adiponectin release (-60%; p < 0.01), and substantially increased leptin (+60%; p < 0.01) and interleukin-6 (+50%; p < 0.001) release. CONCLUSIONS: The hepatokine FGF21 exerts weak lipogenic and anti-adipogenic actions and marked adiponectin-suppressive and leptin and interleukin-6 release-promoting effects in human differentiating preadipocytes. Together with the higher serum concentrations in MUHO subjects, our findings reveal FGF21 as a circulating factor promoting the development of metabolically unhealthy adipocytes.
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In humans, circulating FGF21 levels increase with obesity, type 2 diabetes, and NAFLD.
“In humans, circulating FGF21 levels also increase with obesity [[174], [175], [176]], type 2 diabetes [[176], [177], [178]], and NAFLD [179,180]”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [175]
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- Authors
- Berti, L., Irmler, M., Zdichavsky, M., Meile, T., Böhm, A., Stefan, N., Fritsche, A., Beckers, J., Königsrainer, A., Häring, H.-U., de Angelis, M. H., & Staiger, H.
- Affiliations
- Helmholtz Munich (DE)
- Universitätsklinikum Tübingen (DE)
- Corresponding author
- Staiger, Harald
- ORCID
- Venue
- Molecular Metabolism
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 4
- Issue
- 7
- Pages
- 519-527
- ISSN
- 2212-8778 (ISSN-L)
- PMC
- PMC4481465
- OpenAlex
- W2019864042
- Cited by
- 73
- References
- 45
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 4 · 2023: 1 · 2022: 9 · 2021: 3 · 2020: 8 · 2019: 8 · 2018: 8 · 2017: 5 · 2016: 14 · 2015: 5
- FWCI
- 4.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Metabolism (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion, cc-by-nc-nd)
- Site cant be reached (submittedVersion, cc-by-nc-nd)
- Funders
- Deutsche Forschungsgemeinschaft (STE 1096/3-1)
- Bundesministerium für Bildung und Forschung
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- FGF21, metabolically unhealthy obesity, metabolically healthy obesity, adipogenesis, lipid accumulation, adipokine secretion, adiponectin, leptin, interleukin-6, PPARγ, CEBPA, insulin sensitivity, hepatokines
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