Evidence map›Paper›PMID 28821663›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

AgRP Neurons Can Increase Food Intake during Conditions of Appetite Suppression and Inhibit Anorexigenic Parabrachial Neurons.

Rachel A Essner, Alison G Smith, Adam A Jamnik, Anna R Ryba, Zoe D Trutner, Matthew E Carter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

76 citing papers in PubMed, 127 citations in OpenAlex.

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  19. Knockdown ofFrontiers in physiology · 2025
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16 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Rachel A EssnerDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.
Alison G SmithDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.ORCID 0000-0002-9402-7786
Adam A JamnikDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.
Anna R RybaDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.
Zoe D TrutnerDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.ORCID 0000-0002-2226-4192
Matthew E CarterDepartment of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267 mc10@williams.edu.
Williams College · US

Funding

Determination of how orexigenic AgRP neurons anatomically and functionally interact with anorexigenic PBel CGRP neurons to regulate food intake behaviorR15DK105510 · NIDDK · WILLIAMS COLLEGE · PI CARTER, MATTHEW E · 2015 to 2018
$731k
NIDDK NIH HHS R15 DK105510
6 · The paper itself

Abstract

To maintain energy homeostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functionally interact to regulate food intake. Within the hypothalamus, neurons that express agouti-related protein (AgRP) sense orexigenic factors and orchestrate an increase in food-seeking behavior. In contrast, calcitonin gene-related peptide (CGRP)-expressing neurons in the parabrachial nucleus (PBN) suppress feeding. PBN CGRP neurons become active in response to anorexigenic hormones released following a meal, including amylin, secreted by the pancreas, and cholecystokinin (CCK), secreted by the small intestine. Additionally, exogenous compounds, such as lithium chloride (LiCl), a salt that creates gastric discomfort, and lipopolysaccharide (LPS), a bacterial cell wall component that induces inflammation, exert appetite-suppressing effects and activate PBN CGRP neurons. The effects of increasing the homeostatic drive to eat on feeding behavior during appetite suppressing conditions are unknown. Here, we show in mice that food deprivation or optogenetic activation of AgRP neurons induces feeding to overcome the appetite suppressing effects of amylin, CCK, and LiCl, but not LPS. AgRP neuron photostimulation can also increase feeding during chemogenetic-mediated stimulation of PBN CGRP neurons. AgRP neuron stimulation reduces Fos expression in PBN CGRP neurons across all conditions. Finally, stimulation of projections from AgRP neurons to the PBN increases feeding following administration of amylin, CCK, and LiCl, but not LPS. These results demonstrate that AgRP neurons are sufficient to increase feeding during noninflammatory-based appetite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food intake during homeostatic need.

Indexed as

Appetite RegulationEatingNeural InhibitionAgouti-Related ProteinAnimalsAnorexiaHypothalamusMaleMiceMice, Inbred C57BLMice, TransgenicNeuronsParabrachial NucleusAgouti-Related ProteinAgrp protein, mouseAgRPappetiteCGRPChR2food intakeparabrachial nucleus

Identifiers

PMID28821663
PMCPMC5588461
OpenAlexW2742520311

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.