Evidence map›Paper›PMID 32532003›Full record

ArticleInternational journal of molecular sciences2020

Physiological Disturbance in Fatty Liver Energy Metabolism Converges on IGFBP2 Abundance and Regulation in Mice and Men.

Pia Fahlbusch, Birgit Knebel, Tina Hörbelt, David Monteiro Barbosa, Aleksandra Nikolic, Sylvia Jacob, Hadi Al-Hasani, Frederique Van de Velde, Yves Van Nieuwenhove, Dirk Müller-Wieland and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  10. Multi-omics characterization of type 2 diabetes associated genetic variation.medRxiv : the preprint server for health sciences · 2024
    Article
  11. Article
  12. FGF1 ameliorates obesity-associated hepatic steatosis by reversing IGFBP2 hypermethylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  13. Article
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  15. Comparative Proteomic Analysis of Liver Tissues and Serum inInternational 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

13 authors at 3 institutions in 2 countries.

Pia FahlbuschInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Birgit KnebelInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.ORCID 0000-0002-5575-4315
Tina HörbeltInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
David Monteiro BarbosaInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Aleksandra NikolicInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Sylvia JacobInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Hadi Al-HasaniInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Frederique Van de VeldeDepartment of Endocrinology, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0003-4574-3396
Yves Van NieuwenhoveDepartment of Gastrointestinal Surgery, Ghent University Hospital, 9000 Ghent, Belgium.
Dirk Müller-WielandClinical Research Centre, Department of Internal Medicine I, University Hospital Aachen, 52074 Aachen, Germany.
Bruno LapauwDepartment of Endocrinology, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0002-1584-4965
D Margriet OuwensInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Jorg KotzkaInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center (DDZ), Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.ORCID 0000-0003-1173-9372
Deutsches Diabetes-Zentrum e.V. · DEGhent University Hospital · BEUniversitätsklinikum Aachen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatty liver occurs from simple steatosis with accumulated hepatic lipids and hepatic insulin resistance to severe steatohepatitis, with aggravated lipid accumulation and systemic insulin resistance, but this progression is still poorly understood. Analyses of hepatic gene expression patterns from alb-SREBP-1c mice with moderate, or aP2-SREBP-1c mice with aggravated, hepatic lipid accumulation revealed IGFBP2 as key nodal molecule differing between moderate and aggravated fatty liver. Reduced IGFBP2 expression in aggravated fatty liver was paralleled with promoter hypermethylation, reduced hepatic IGFBP2 secretion and IGFBP2 circulating in plasma. Physiologically, the decrease of IGFBP2 was accompanied with reduced fatty acid oxidation and increased de novo lipogenesis potentially mediated by IGF1 in primary hepatocytes. Furthermore, methyltransferase and sirtuin activities were enhanced. In humans, IGFBP2 serum concentration was lower in obese men with non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) compared to non-obese controls, and liver fat reduction by weight-loss intervention correlated with an increase of IGFBP2 serum levels. In conclusion, hepatic IGFBP2 abundance correlates to its circulating level and is related to hepatic energy metabolism and de novo lipogenesis. This designates IGFBP2 as non-invasive biomarker for fatty liver disease progression and might further provide an additional variable for risk prediction for pathogenesis of fatty liver in diabetes subtype clusters.

Indexed as

AdultAnimalsBody WeightCase-Control StudiesEnergy MetabolismHepatocytesHumansInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IInsulin ResistanceMaleMice, Inbred C57BLMice, TransgenicMiddle AgedNon-alcoholic Fatty Liver DiseaseIGF1 protein, humanIGFBP2 protein, humanIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor ISrebf1 protein, mouseSterol Regulatory Element Binding Protein 1de novo lipogenesisfatty liver metabolismfatty liver progressionIGFBP2IGF systemmethylationNAFLDSREBP-1c

Identifiers

PMID32532003
PMCPMC7312731
OpenAlexW3034450739

What OpenQuestion holds

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LicenceCC BY
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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.