Evidence map›Paper›PMID 39017739›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Kinin B1 receptor deficiency promotes enhanced adipose tissue thermogenic response to β3-adrenergic stimulation.

Jéssica Branquinho, Raquel L Neves, Renan P Martin, Júlia G Arata, Clarissa A Bittencourt, Ronaldo C Araújo, Marcelo Y Icimoto, João B Pesquero

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Kinin receptors in adipose tissue: drivers of inflammation and metabolic dysfunction in obesity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

8 authors.

Jéssica BranquinhoCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Raquel L NevesCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Renan P MartinCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Júlia G ArataCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Clarissa A BittencourtCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Ronaldo C AraújoDepartment of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil.
Marcelo Y IcimotoDepartment of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil. icimoto@unifesp.br.
João B PesqueroCenter for Research and Molecular Diagnostic of Genetic Diseases, Department of Biophysics, Federal University of São Paulo, São Paulo, SP, Brazil. jbpesquero@unifesp.br.

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 142138/2017-7Conselho Nacional de Desenvolvimento Científico e Tecnológico 432165/2021-6Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/27198-8
6 · The paper itself

Abstract

OBJECTIVE AND

designKinin B1 receptor (B1R) has a key role in adipocytes to protect against obesity and glycemic metabolism, thus becoming a potential target for regulation of energy metabolism and adipose tissue thermogenesis. MATERIAL OR SUBJECTS: Kinin B1 knockout mice (B1KO) were subjected to acute induction with CL 316,243 and chronic cold exposure.

methodsMetabolic and histological analyses, gene and protein expression and RNA-seq were performed on interscapular brown adipose tissue (iBAT) and inguinal white adipose tissue (iWAT) of mice.

resultsB1KO mice, under acute effect of CL 316,243, exhibited increased energy expenditure and upregulated thermogenic genes in iWAT. They were also protected from chronic cold, showing enhanced non-shivering thermogenesis with increased iBAT mass (~ 90%) and recruitment of beige adipocytes in iWAT (~ 50%). Positive modulation of thermogenic and electron transport chain genes, reaching a 14.5-fold increase for Ucp1 in iWAT. RNA-seq revealed activation of the insulin signaling pathways for iBAT and oxidative phosphorylation, tricarboxylic acid cycle, and browning pathways for iWAT.

conclusionB1R deficiency induced metabolic and gene expression alterations in adipose tissue, activating thermogenic pathways and increasing energy metabolism. B1R antagonists emerge as promising therapeutic targets for regulating obesity and associated metabolic disorders, such as inflammation and diabetes.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteDioxolesMice, KnockoutReceptor, Bradykinin B1ThermogenesisAdrenergic beta-3 Receptor AgonistsAnimalsCold TemperatureEnergy MetabolismMaleMiceMice, Inbred C57BLReceptors, Adrenergic, beta-3ThiazolesUncoupling Protein 1Adrb3 protein, mouseAdrenergic beta-3 Receptor AgonistsDioxolesdisodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylateReceptor, Bradykinin B1Receptors, Adrenergic, beta-3ThiazolesUncoupling Protein 1AdipocyteAdipose tissueKininsMetabolic diseasesMetabolismThermogenesis

Identifiers

PMID39017739

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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.