Evidence map›Paper›PMID 29467502›Full record

ArticleInternational journal of obesity (2005)2018

CDH13 abundance interferes with adipocyte differentiation and is a novel biomarker for adipose tissue health.

Simon Göddeke, Birgit Knebel, Pia Fahlbusch, Tina Hörbelt, Gereon Poschmann, Frederique van de Velde, Tim Benninghoff, Hadi Al-Hasani, Sylvia Jacob, Yves Van Nieuwenhove and 4 more

Abstract read
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In one paragraph

Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

18 citing papers in PubMed, 27 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 3 institutions in 2 countries.

Simon GöddekeInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Birgit KnebelInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.ORCID http://orcid.org/0000-0002-5575-4315
Pia FahlbuschInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Tina HörbeltInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Gereon PoschmannMolecular Proteomics Laboratory, Biomedizinisches Forschungszentrum (BMFZ), Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany.
Frederique van de VeldeDepartment of Endocrinology, Ghent University Hospital, Ghent, Belgium.
Tim BenninghoffInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Hadi Al-HasaniInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Sylvia JacobInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Yves Van NieuwenhoveDepartment of Gastrointestinal Surgery, Ghent University Hospital, Ghent, Belgium.
Bruno LapauwDepartment of Endocrinology, Ghent University Hospital, Ghent, Belgium.
Stefan LehrInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
D Margriet OuwensInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany.
Jorg KotzkaInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Aufm Hennekamp 65, 40225, Duesseldorf, Germany. joerg.kotzka@ddz.uni-duesseldorf.de.ORCID http://orcid.org/0000-0003-1173-9372
Deutsches Diabetes-Zentrum e.V. · DEGhent University Hospital · BEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCDH13, an atypical member of the cadherin superfamily, has been identified in adipocyte secretomes of lean mouse models. CDH13 abundance differs in mouse models according to their susceptibility to develop metabolic disorders, but the role of CDH13 in adipose tissue is unknown.

methodsSecreted CDH13 protein levels and mRNA levels in visceral adipose tissue were determined in lean and obese mouse models. In vitro studies were performed in 3T3-L1 adipocytes to determine the role of CDH13 in adipocyte differentiation. The pathophysiological impact of visceral adipose tissue CDH13 mRNA and circulating CDH13 levels were determined in humans (normal-weight men n = 37, obese men n = 109 including n = 51 type 2 diabetes patients) and in obese patients (n = 14) pre- and post-metabolic surgery.

resultsThis study shows that in visceral adipose tissue CDH13 protein secretion and mRNA levels were decreased in obese mouse models. Mechanistically, CDH13 affects lipid metabolism during adipogenesis but not in mature adipocytes. CDH13 knockdown during adipogenesis reduced fatty acid uptake and lipid content in developing adipocytes. Furthermore, CDH13 depletion during adipogenesis lowered the induction of PPARγ and C/EBPα expression. These observations are of pathophysiological impact since visceral adipose tissue CDH13 mRNA and circulating CDH13 levels were decreased in obese men compared to normal-weight controls. Weight loss induced by bariatric surgery restored circulating CDH13 to levels found in normal-weight controls.

conclusionsCDH13 levels in adipose tissue and the circulation are affected by obesity in mouse models and humans and are restored by weight loss in humans. CDH13 interferes with the differentiation potential of adipocytes and therefore is a marker for plasticity of fat tissue that might reflect the health status of adipose tissue.

Indexed as

AdipocytesAdipogenesisAdipose TissueAdultAnimalsBiomarkersCadherinsCell DifferentiationFemaleHumansMaleMiceMice, ObeseMiddle AgedObesityRNA, MessengerBiomarkersCadherinsH-cadherinRNA, Messenger

Identifiers

PMID29467502
OpenAlexW2794073447

What OpenQuestion holds

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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.