Evidence map›Paper›PMID 26936779›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats.

Alison D Kreisler, Linda Rinaman

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

25 citing papers in PubMed, 28 citations in OpenAlex.

  1. Cellular coding of ingestion in the caudal brainstem.bioRxiv : the preprint server for biology · 2026
    Article
  2. GLP-1 physiology and pharmacology along the gut-brain axis.The Journal of clinical investigation · 2026
    Review
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  7. Molecular Ontology of the Nucleus of Solitary Tract.The Journal of comparative neurology · 2024
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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

2 authors at 1 institution in 1 country.

Alison D KreislerDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania.
Linda RinamanDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania rinaman@pitt.edu.
University of Pittsburgh · US

Funding

POSTNATAL DEVELOPMENT OF VAGAL-HYPOTHALAMIC CONNECTIONSR01MH059911 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINAMAN, LINDA M · 1999 to 2024
$7.3M
Brainstem Satiety Circuits and High Fat Diet HyperphagiaR01DK100685 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINAMAN, LINDA M · 2014 to 2018
$1.6M
NIDDK NIH HHS R01 DK100685NIMH NIH HHS R01 MH059911
6 · The paper itself

Abstract

Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ∼11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ∼14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.

Indexed as

Stress, PhysiologicalAcclimatizationAnimalsDietary SucroseEatingFood, FormulatedGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorMealsNeuronsPeptide FragmentsRatsRhombencephalonTime FactorsDietary SucroseEnsure formulated foodexendin (9-39)Glucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorPeptide FragmentscFosExendin-3 (9–39), Ex9meal patterns

Identifiers

PMID26936779
PMCPMC4896082
OpenAlexW2321474412

What OpenQuestion holds

Textmetadata
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.