Evidence map›Paper›PMID 29980484›Full record

ArticleMolecular metabolism2018

FGF21 regulates insulin sensitivity following long-term chronic stress.

Tomas Jelenik, Matthias Dille, Sabrina Müller-Lühlhoff, Dhiraj G Kabra, Zhou Zhou, Christian Binsch, Sonja Hartwig, Stefan Lehr, Alexandra Chadt, Eva M J Peters and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

23 citing papers in PubMed, 26 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Tomas JelenikInstitute for Clinical Diabetology, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Matthias DilleInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Sabrina Müller-LühlhoffInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Dhiraj G KabraInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Zhou ZhouInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Christian BinschInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Sonja HartwigInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Stefan LehrInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Alexandra ChadtInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Eva M J PetersJustus-Liebig-University, Department of Psychosomatics and Psychotherapy, Psychoneuroimmunology Laboratory, Gießen, Germany.
Johannes KruseJustus-Liebig-University, Department of Psychosomatics and Psychotherapy, Psychoneuroimmunology Laboratory, Gießen, Germany.
Michael RodenInstitute for Clinical Diabetology, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany; Division of Endocrinology and Diabetology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.
Hadi Al-HasaniInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany. Electronic address: hadi.al-hasani@ddz.uni-duesseldorf.de.
Tamara R CastañedaInstitute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Medical Faculty, Heinrich Heine University, Leibniz Center for Diabetes Research, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.
Deutsches Diabetes-Zentrum e.V. · DEJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePost-traumatic stress disorder (PTSD) increases type 2 diabetes risk, yet the underlying mechanisms are unclear. We investigated how early-life exposure to chronic stress affects long-term insulin sensitivity.

methodsC57Bl/6J mice were exposed to chronic variable stress for 15 days (Cvs) and then recovered for three months without stress (Cvs3m).

resultsCvs mice showed markedly increased plasma corticosterone and hepatic insulin resistance. Cvs3m mice exhibited improved whole-body insulin sensitivity along with enhanced adipose glucose uptake and skeletal muscle mitochondrial function and fatty acid oxidation. Plasma FGF21 levels were substantially increased and associated with expression of genes involved in fatty acid oxidation and formation of brown-like adipocytes. In humans, serum FGF21 levels were associated with stress coping long time after the exposure.

conclusionsEarly-life exposure to chronic stress leads to long term improvements in insulin sensitivity, oxidative metabolism and adipose tissue remodeling. FGF21 contributes to a physiological memory mechanism to maintain metabolic homeostasis.

Indexed as

AdipocytesAnimalsDiabetes Mellitus, ExperimentalDisease Models, AnimalEnergy MetabolismFibroblast Growth FactorsGlucoseHomeostasisInsulinInsulin ResistanceLipid MetabolismLiverMaleMiceMice, Inbred C57BLObesityfibroblast growth factor 21Fibroblast Growth FactorsGlucoseInsulinChronic variable stressDiabetesFGF21Insulin sensitivityPTSDWhite adipose tissue

Identifiers

PMID29980484
PMCPMC6158095
OpenAlexW2809658288

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.