Evidence map›Paper›PMID 32603548›Full record

ArticleActa physiologica (Oxford, England)2021

Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet.

Molly McDougle, Danielle Quinn, Charlene Diepenbroek, Arashdeep Singh, Claire de la Serre, Guillaume de Lartigue

Open access · hybridAbstract read
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Article in Acta physiologica (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  7. Cholinergic Neurotransmission Controls Orexigenic Endocannabinoid Signaling in the Gut in Diet-Induced Obesity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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  10. Review
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  15. Nutrient-Based Appetite Regulation.Journal of obesity & metabolic syndrome · 2022
    Review
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  19. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Molly McDougleDepartment of Pharmacodynamics, University of Florida, Gainesville, FL, USA.
Danielle QuinnThe John B. Pierce Laboratory, New Haven, CT, USA.
Charlene DiepenbroekThe John B. Pierce Laboratory, New Haven, CT, USA.
Arashdeep SinghDepartment of Pharmacodynamics, University of Florida, Gainesville, FL, USA.
Claire de la SerreDepartment of Foods and Nutrition, University of Georgia, Athens, GA, USA.
Guillaume de LartigueDepartment of Pharmacodynamics, University of Florida, Gainesville, FL, USA.ORCID 0000-0002-0032-8810
University of Florida Health · USJohn B. Pierce Laboratory · USUniversity of Georgia · USYale University · US

Funding

Evaluating the therapeutic potential of vagal CART circuitry for treating metabolic diseaseR01DK116004 · NIDDK · UNIVERSITY OF FLORIDA · PI Guillaume FH de Lartigue · 2018 to 2026
$3.6M
Consequence and mechanism of diet-driven vagal remodeling on gut-brain feedingbehaviorR01DK125890 · NIDDK · UNIVERSITY OF GEORGIA · PI DE LA SERRE, CLAIRE, DE LARTIGUE, GUILLAUME FH · 2020 to 2023
$1.8M
The role of vagal afferent neurons in regulating feeding behaviorR00DK094871 · NIDDK · JOHN B. PIERCE LABORATORY, INC. · PI DE LARTIGUE, GUILLAUME FH · 2015 to 2017
$718k
Microbiome-Vagal-Brain signaling: impact on the reward system and food intakeR21DK110511 · NIDDK · UNIVERSITY OF GEORGIA · PI DE LA SERRE, CLAIRE · 2016 to 2017
$435k
NIDDK NIH HHS R00 DK094871NIDDK NIH HHS R01 DK116004NIDDK NIH HHS R01 DK125890NIDDK NIH HHS R21 DK110511
6 · The paper itself

Abstract

aimThe tools that have been used to assess the function of the vagus nerve lack specificity. This could explain discrepancies about the role of vagal gut-brain signalling in long-term control of energy balance. Here we use a validated approach to selectively ablate sensory vagal neurones that innervate the gut to determine the role of vagal gut-brain signalling in the control of food intake, energy expenditure and glucose homoeostasis in response to different diets.

methodsRat nodose ganglia were injected bilaterally with either the neurotoxin saporin conjugated to the gastrointestinal hormone cholecystokinin (CCK), or unconjugated saporin as a control. Food intake, body weight, glucose tolerance and energy expenditure were measured in both groups in response to chow or high-fat high-sugar (HFHS) diet. Willingness to work for fat or sugar was assessed by progressive ratio for orally administered solutions, while post-ingestive feedback was tested by measuring food intake after an isocaloric lipid or sucrose pre-load.

resultsVagal deafferentation of the gut increases meal number in lean chow-fed rats. Switching to a HFHS diet exacerbates overeating and body weight gain. The breakpoint for sugar or fat solution did not differ between groups, suggesting that increased palatability may not drive HFHS-induced hyperphagia. Instead, decreased satiation in response to intra-gastric infusion of fat, but not sugar, promotes hyperphagia in CCK-Saporin-treated rats fed with HFHS diet.

conclusionsWe conclude that intact sensory vagal neurones prevent hyperphagia and exacerbation of weight gain in response to a HFHS diet by promoting lipid-mediated satiation.

Indexed as

HyperphagiaSugarsAnimalsBrainDiet, High-FatRatsVagus NerveWeight GainSugarsfatobesitypalatabilitypost-ingestivesugarvagus nerve

Identifiers

PMID32603548
PMCPMC7772266
OpenAlexW3038391429

What OpenQuestion holds

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LicenceCC BY
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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.