Evidence map›Paper›PMID 26137439›Full record

ArticleMolecular metabolism2015

Fibroblast growth factor 21 is elevated in metabolically unhealthy obesity and affects lipid deposition, adipogenesis, and adipokine secretion of human abdominal subcutaneous adipocytes.

Lucia Berti, Martin Irmler, Marty Zdichavsky, Tobias Meile, Anja Böhm, Norbert Stefan, Andreas Fritsche, Johannes Beckers, Alfred Königsrainer, Hans-Ulrich Häring and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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  13. Curcumin and Weight Loss: Does It Work?International journal of molecular sciences · 2022
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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

12 authors at 4 institutions in 1 country.

Lucia BertiInstitute of Experimental Genetics, Helmholtz Centre Munich GmbH, German Research Centre for Environmental Health, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; German Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany.
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Centre Munich GmbH, German Research Centre for Environmental Health, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; German Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany.
Marty ZdichavskyDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Hoppe-Seyler-Straße 3, D-72076 Tübingen, Germany.
Tobias MeileDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Hoppe-Seyler-Straße 3, D-72076 Tübingen, Germany.
Anja BöhmGerman Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany ; Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany.
Norbert StefanGerman Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany ; Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany.
Andreas FritscheGerman Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany ; Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany.
Johannes BeckersInstitute of Experimental Genetics, Helmholtz Centre Munich GmbH, German Research Centre for Environmental Health, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; German Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Chair for Experimental Genetics, Technical University Munich, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany.
Alfred KönigsrainerDepartment of General, Visceral and Transplant Surgery, University Hospital Tübingen, Hoppe-Seyler-Straße 3, D-72076 Tübingen, Germany.
Hans-Ulrich HäringGerman Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany ; Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany.
Martin Hrabě de AngelisInstitute of Experimental Genetics, Helmholtz Centre Munich GmbH, German Research Centre for Environmental Health, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; German Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Chair for Experimental Genetics, Technical University Munich, Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany.
Harald StaigerGerman Centre for Diabetes Research (DZD), Ingolstädter Landstraße 1, D-85764 Neuherberg, Germany ; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany ; Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany.
Heinrich Heine University Düsseldorf · DEHelmholtz Zentrum München · DEGerman Center for Diabetes Research · DEDeutsches Diabetes-Zentrum e.V. · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSerum 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.

methodsIn 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.

resultsSerum 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.

conclusionsThe 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.

Indexed as

AdipokineAdiponectinAMPK, AMP-activated protein kinaseBMI, body mass indexC/EBP-α, CCAAT/enhancer-binding protein-αCIDEA, cell death-inducing DNA fragmentation factor-like effector aERK, extracellular signal-regulated kinaseFGF21FGF, fibroblast growth factorGAPDH, glyceraldehyde 3-phosphate dehydrogenasehasc, human abdominal subcutaneousHepatokineIL-6, interleukin-6MHO, metabolically healthy obesityMUHO, metabolically unhealthy obesityPGC-1α, PPAR-γ coactivator-1αPPAR-γ, peroxisome proliferator-activated receptor-γqPCR, quantitative polymerase chain reactionrh, recombinant humanSecretomeType-2 diabetesUCP-1, uncoupling protein-1

Identifiers

PMID26137439
PMCPMC4481465
OpenAlexW2019864042

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LicenceCC BY-NC-ND
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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.