Evidence map›Paper›PMID 29107299›Full record

ArticleMolecular metabolism2017

Bombesin-like receptor 3 (Brs3) expression in glutamatergic, but not GABAergic, neurons is required for regulation of energy metabolism.

Cuiying Xiao, Ramón A Piñol, Jesse Lea Carlin, Cuiling Li, Chuxia Deng, Oksana Gavrilova, Marc L Reitman

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Using thermal preference to understand mouse thermal biology.American journal of physiology. Endocrinology and metabolism · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Cuiying XiaoDiabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Ramón A PiñolDiabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Jesse Lea CarlinDiabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Cuiling LiGenetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Chuxia DengGenetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA; Faculty of Health Sciences, University of Macau, Macau SAR, China.
Oksana GavrilovaMouse Metabolism Core, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
Marc L ReitmanDiabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA. Electronic address: marc.reitman@nih.gov.
National Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Macau · MO

Funding

What can body temperature tell us about energy homeostasis?ZIADK075063 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI REITMAN, MARC L · 2012 to 2025
$5.6M
Pharmacologic approaches to the treatment of obesityZIADK075062 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI REITMAN, MARC L · 2012 to 2025
$5.5M
6 · The paper itself

Abstract

objectiveBombesin-like receptor 3 (BRS-3) is an orphan G protein-coupled receptor. Brs3 null mice have reduced resting metabolic rate and body temperature, increased food intake, and obesity. Here we study the role of Brs3 in different neuron types.

methodsMice able to undergo Cre recombinase-dependent inactivation or re-expression of Brs3 were generated, respectively Brs3

resultsDeletion of Brs3 in glutamatergic neurons expressing Vglut2 reproduced the global null phenotype for regulation of food intake, metabolic rate, body temperature, adiposity, and insulin resistance. These mice also no longer responded to a BRS-3 agonist, MK-5046. In contrast, deletion of Brs3 in GABAergic neurons produced no detectable phenotype. Conversely, the wild type phenotype was restored by selective re-expression of Brs3 in glutamatergic neurons, with no normalization achieved by re-expressing Brs3 in GABAergic neurons.

conclusionsBrs3 expression in glutamatergic neurons is both necessary and sufficient for full Brs3 function in energy metabolism. In these experiments, no function was identified for Brs3 in GABAergic neurons. The data suggest that the anti-obesity pharmacologic actions of BRS-3 agonists occur via agonism of receptors on glutamatergic neurons.

Indexed as

AdiposityAnimalsBody WeightEatingEnergy MetabolismGABAergic NeuronsGene ExpressionGlutamic AcidImidazolesMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsObesityPyrazoles1,1,1-trifluoro-2-(4-(1H-pyrazol-1-yl)phenyl)-3-(4-((1-(trifluoromethyl)cyclopropyl)methyl)-1H-imidazol-2-yl)propan-2-olbombesin receptor subtype 3Glutamic AcidImidazolesPyrazolesReceptors, BombesinBody temperatureBombesin-like receptor 3Energy expenditureFood intakeGlutamatergic neuronsObesity

Identifiers

PMID29107299
PMCPMC5681273
OpenAlexW2755835009

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.