Evidence map›Paper›PMID 36433953›Full record

ArticleNature communications2022

Reduced secretion of neuronal growth regulator 1 contributes to impaired adipose-neuronal crosstalk in obesity.

Elisa Duregotti, Christina M Reumiller, Ursula Mayr, Maria Hasman, Lukas E Schmidt, Sean A Burnap, Konstantinos Theofilatos, Javier Barallobre-Barreiro, Arne Beran, Maria Grandoch and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  8. From fasting to fat reshaping: exploring the molecular pathways of intermittent fasting-induced adipose tissue remodeling.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
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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.

Elisa DuregottiKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0003-1409-4063
Christina M ReumillerKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0001-9072-259X
Ursula MayrKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.
Maria HasmanKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0003-4512-0025
Lukas E SchmidtKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0001-7565-1455
Sean A BurnapKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0002-3408-8608
Konstantinos TheofilatosKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.ORCID 0000-0001-6799-0553
Javier Barallobre-BarreiroKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK.
Arne BeranInstitute of Translational Pharmacology, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Maria GrandochInstitute of Translational Pharmacology, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Alessandro VivianoDepartment of Cardiothoracic Surgery, St. George's Hospital, University of London, London, UK.
Marjan JahangiriDepartment of Cardiothoracic Surgery, St. George's Hospital, University of London, London, UK.
Manuel MayrKing's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences, London, UK. manuel.mayr@kcl.ac.uk.ORCID 0000-0002-0597-829X
King's College London · GBDüsseldorf University Hospital · DEUniversity of London · GB

Funding

British Heart Foundation RG/16/14/32397British Heart Foundation RG/F/21/110053
6 · The paper itself

Abstract

While the endocrine function of white adipose tissue has been extensively explored, comparatively little is known about the secretory activity of less-investigated fat depots. Here, we use proteomics to compare the secretory profiles of male murine perivascular depots with those of canonical white and brown fat. Perivascular secretomes show enrichment for neuronal cell-adhesion molecules, reflecting a higher content of intra-parenchymal sympathetic projections compared to other adipose depots. The sympathetic innervation is reduced in the perivascular fat of obese (ob/ob) male mice, as well as in the epicardial fat of patients with obesity. Degeneration of sympathetic neurites is observed in presence of conditioned media of fat explants from ob/ob mice, that show reduced secretion of neuronal growth regulator 1. Supplementation of neuronal growth regulator 1 reverses this neurodegenerative effect, unveiling a neurotrophic role for this protein previously identified as a locus associated with human obesity. As sympathetic stimulation triggers energy-consuming processes in adipose tissue, an impaired adipose-neuronal crosstalk is likely to contribute to the disrupted metabolic homeostasis characterising obesity.

Indexed as

Adipose Tissue, BrownObesityAdipose Tissue, WhiteAnimalsHumansMaleMiceMice, Obese

Identifiers

PMID36433953
PMCPMC9700863
OpenAlexW4310058914

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.