Evidence map›Paper›PMID 35662413›Full record

ArticleCell2022

An inter-organ neural circuit for appetite suppression.

Tong Zhang, Matthew H Perkins, Hao Chang, Wenfei Han, Ivan E de Araujo

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
16.1field-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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 160 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 2 countries.

Tong ZhangNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA; Department of Colorectal Surgery, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510180, China; Jinan University, Guangzhou, Guangdong 510632, China.
Matthew H PerkinsNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA.
Hao ChangNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA.
Wenfei HanNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA. Electronic address: wenfei.han@mssm.edu.
Ivan E de AraujoNash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA; Artificial Intelligence and Emerging Technologies in Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA; Diabetes, Obesity and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA. Electronic address: ivan.dearaujo@mssm.edu.
Icahn School of Medicine at Mount Sinai · US

Funding

Spinal Sensory Ganglia and Gut SensationR01AT011697 · NCCIH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DE ARAUJO, IVAN E, PERKINS, MATTHEW HUNTOON · 2021 to 2025
$2.9M
Molecular and Cellular Basis of the Gut-Brain Axis in Parkinsons DiseaseP20NS123220 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU · 2021 to 2022
$1.0M
NCCIH NIH HHS R01 AT011697NINDS NIH HHS P20 NS123220
6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) is a signal peptide released from enteroendocrine cells of the lower intestine. GLP-1 exerts anorectic and antimotility actions that protect the body against nutrient malabsorption. However, little is known about how intestinal GLP-1 affects distant organs despite rapid enzymatic inactivation. We show that intestinal GLP-1 inhibits gastric emptying and eating via intestinofugal neurons, a subclass of myenteric neurons that project to abdominal sympathetic ganglia. Remarkably, cell-specific ablation of intestinofugal neurons eliminated intestinal GLP-1 effects, and their chemical activation functioned as a GLP-1 mimetic. GLP-1 sensing by intestinofugal neurons then engaged a sympatho-gastro-spinal-reticular-hypothalamic pathway that links abnormal stomach distension to craniofacial programs for food rejection. Within this pathway, cell-specific activation of discrete neuronal populations caused systemic GLP-1-like effects. These molecularly identified, delimited enteric circuits may be targeted to ameliorate the abdominal bloating and loss of appetite typical of gastric motility disorders.

Indexed as

AppetiteIleumNeuronsStomachAbdomenAnimalsCell CommunicationGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorMaleMiceNitric OxideSignal TransductionGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorNitric OxideAppetite suppressionenteric neuronsGLP-1gut-brain axisgut peptidesinteroception

Identifiers

PMID35662413
PMCPMC9433108
OpenAlexW4281724694

What OpenQuestion holds

Textmetadata
LicenceTDM
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.