Evidence map›Paper›PMID 36847494›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2023

Hindbrain ghrelin and liver-expressed antimicrobial peptide 2, ligands for growth hormone secretagogue receptor, bidirectionally control food intake.

Hallie S Wald, Misgana Y Ghidewon, Matthew R Hayes, Harvey J Grill

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
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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

4 authors at 1 institution in 1 country.

Hallie S WaldDepartment of Psychology, Institute of Diabetes Obesity and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, United States.ORCID 0000-0002-8195-9488
Misgana Y GhidewonDepartment of Psychology, Institute of Diabetes Obesity and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, United States.
Matthew R HayesDepartment of Psychiatry, Institute of Diabetes Obesity and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States.
Harvey J GrillDepartment of Psychology, Institute of Diabetes Obesity and Metabolism, University of Pennsylvania, Philadelphia, Pennsylvania, United States.ORCID 0000-0003-3290-3784
University of Pennsylvania · US

Funding

NEURAL HIERARCHY IN THE MODULATION OF INGESTIVE BEHAVIORR01DK021397 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GRILL, HARVEY J, HAYES, MATTHEW R · 1986 to 2021
$8.8M
Neurobehavioral correlates of individual differences in obesity susceptibilityF31DK120162 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI WALD, HALLIE S · 2018 to 2020
$148k
NIDDK NIH HHS F31 DK120162NIDDK NIH HHS R01 DK021397
6 · The paper itself

Abstract

Hindbrain growth hormone secretagogue receptor (GHSR) agonism increases food intake, yet the underlying neural mechanisms remain unclear. The functional effects of hindbrain GHSR antagonism by its endogenous antagonist liver-expressed antimicrobial peptide 2 (LEAP2) are also yet unexplored. To test the hypothesis that hindbrain GHSR agonism attenuates the food intake inhibitory effect of gastrointestinal (GI) satiation signals, ghrelin (at a feeding subthreshold dose) was administered to the fourth ventricle (4V) or directly to the nucleus tractus solitarius (NTS) before systemic delivery of the GI satiation signal cholecystokinin (CCK). Also examined, was whether hindbrain GHSR agonism attenuated CCK-induced NTS neural activation (c-Fos immunofluorescence). To investigate an alternate hypothesis that hindbrain GHSR agonism enhances feeding motivation and food seeking, intake stimulatory ghrelin doses were administered to the 4V and fixed ratio 5 (FR-5), progressive ratio (PR), and operant reinstatement paradigms for palatable food responding were evaluated. Also assessed were 4V LEAP2 delivery on food intake and body weight (BW) and on ghrelin-stimulated feeding. Both 4V and NTS ghrelin blocked the intake inhibitory effect of CCK and 4V ghrelin blocked CCK-induced NTS neural activation. Although 4V ghrelin increased low-demand FR-5 responding, it did not increase high-demand PR or reinstatement of operant responding. Fourth ventricle LEAP2 reduced chow intake and BW and blocked hindbrain ghrelin-stimulated feeding. Data support a role for hindbrain GHSR in bidirectional control of food intake through mechanisms that include interacting with the NTS neural processing of GI satiation signals but not food motivation and food seeking.

Indexed as

HepcidinsReceptors, GhrelinCholecystokininEatingGhrelinSolitary NucleusCholecystokininGhrelinHepcidinsReceptors, Ghrelincholecystokininfood motivationfood seekingghrelin receptorsatiation signals

Identifiers

PMID36847494
PMCPMC10069974
OpenAlexW4322494701

What Socratic 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 Socratic graph.