Evidence map›Paper›PMID 34043943›Full record

ArticleCell metabolism2021

Gut-brain communication by distinct sensory neurons differently controls feeding and glucose metabolism.

Diba Borgmann, Elisa Ciglieri, Nasim Biglari, Claus Brandt, Anna Lena Cremer, Heiko Backes, Marc Tittgemeyer, F Thomas Wunderlich, Jens C Brüning, Henning Fenselau

Open access · hybridAbstract read
In one paragraph

Article in Cell metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 1 pooled it
11.7field-weighted citation impact, top 1% 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

120 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.

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  7. The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026
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60 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Diba BorgmannSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Translational Neurocircuitry Group, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Anatomy II, Neuroanatomy, University Hospital Cologne, Joseph-Stelzmann Str. 9, 50937 Cologne, Germany.
Elisa CiglieriSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50937 Cologne, Germany.
Nasim BiglariMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany.
Claus BrandtMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany.
Anna Lena CremerMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany.
Heiko BackesMax Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany.
Marc TittgemeyerTranslational Neurocircuitry Group, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany.
F Thomas WunderlichCenter for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50937 Cologne, Germany; Max Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany; Center of Molecular Medicine Cologne (CMMC), University of Cologne, Robert-Koch-Straße 21, 50931 Cologne, Germany.
Jens C BrüningCenter for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50937 Cologne, Germany; Max Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Strasse 50, 50931 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany; Center of Molecular Medicine Cologne (CMMC), University of Cologne, Robert-Koch-Straße 21, 50931 Cologne, Germany.
Henning FenselauSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Strasse 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Strasse 26, 50937 Cologne, Germany; Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany. Electronic address: henning.fenselau@sf.mpg.de.
Max Planck Institute for Metabolism Research · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity Hospital Cologne · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sensory neurons relay gut-derived signals to the brain, yet the molecular and functional organization of distinct populations remains unclear. Here, we employed intersectional genetic manipulations to probe the feeding and glucoregulatory function of distinct sensory neurons. We reconstruct the gut innervation patterns of numerous molecularly defined vagal and spinal afferents and identify their downstream brain targets. Bidirectional chemogenetic manipulations, coupled with behavioral and circuit mapping analysis, demonstrated that gut-innervating, glucagon-like peptide 1 receptor (GLP1R)-expressing vagal afferents relay anorexigenic signals to parabrachial nucleus neurons that control meal termination. Moreover, GLP1R vagal afferent activation improves glucose tolerance, and their inhibition elevates blood glucose levels independent of food intake. In contrast, gut-innervating, GPR65-expressing vagal afferent stimulation increases hepatic glucose production and activates parabrachial neurons that control normoglycemia, but they are dispensable for feeding regulation. Thus, distinct gut-innervating sensory neurons differentially control feeding and glucoregulatory neurocircuits and may provide specific targets for metabolic control.

Indexed as

Appetite RegulationAfferent PathwaysAnimalsAppetiteBrain-Gut AxisCell CommunicationEnergy MetabolismGlucagon-Like Peptide-1 ReceptorGlucoseHomeodomain ProteinsMaleMice, TransgenicNodose GanglionReceptors, G-Protein-CoupledSensory Receptor CellsTranscription FactorsGlp1r protein, mouseGlucagon-Like Peptide-1 ReceptorGlucoseGPR65 protein, mouseHomeodomain ProteinsPhox2b protein, mouseReceptors, G-Protein-CoupledTranscription FactorsWnt1 ProteinWnt1 protein, mouseappetitechemogeneticsdorsal root ganglionDre-recombinaseglucose metabolismgut-brain axisintersectional geneticsnodose ganglionsensory neuronsvagus nerve

Identifiers

PMID34043943
PMCPMC8280952
OpenAlexW3165632252

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.