Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease.

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dc.creatorRebeca P. M. Santos
dc.creatorRoberta Ribeiro
dc.creatorTalita H. Ferreira-Vieira
dc.creatorRosaria D. Aires
dc.creatorJessica M. de Souza
dc.creatorBruna S. Oliveira
dc.creatorAnna Luiza D. Lima
dc.creatorAntônio Carlos P. de Oliveira
dc.creatorHelton J. Reis
dc.creatorAline S. de Miranda
dc.creatorErica M. L. Vieira
dc.creatorFabiola M. Ribeiro
dc.creatorLuciene Bruno Vieira
dc.date.accessioned2023-10-30T21:34:16Z
dc.date.accessioned2025-09-09T00:48:08Z
dc.date.available2023-10-30T21:34:16Z
dc.date.issued2022
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1038/s41598-022-08924-4
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/1843/60288
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofScientific Reports
dc.rightsAcesso Aberto
dc.subjectReceptores de Glutamato Metabotrópico 5
dc.subjectObesidade
dc.subjectDoença de Huntington
dc.subjectCamundongos knockout
dc.subject.otherMetabotropic glutamate receptor 5
dc.subject.otherObesity
dc.subject.otherHuntington’s disease
dc.subject.otherKnockout mice
dc.titleMetabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease.
dc.typeArtigo de periódico
local.citation.volume12
local.description.resumoObesity represents a global health problem and is characterized by metabolic dysfunctions and a low-grade chronic inflammatory state, which can increase the risk of comorbidities, such as atherosclerosis, diabetes and insulin resistance. Here we tested the hypothesis that the genetic deletion of metabotropic glutamate receptor 5 (mGluR5) may rescue metabolic and inflammatory features present in BACHD mice, a mouse model of Huntington’s disease (HD) with an obese phenotype. For that, we crossed BACHD and mGluR5 knockout mice (mGluR5−/−) in order to obtain the following groups: Wild type (WT), mGluR5−/−, BACHD and BACHD/mGluR5−/− (double mutant mice). Our results showed that the double mutant mice present decreased body weight as compared to BACHD mice in all tested ages and reduced visceral adiposity as compared to BACHD at 6 months of age. Additionally, 12-month-old double mutant mice present increased adipose tissue levels of adiponectin, decreased leptin levels, and increased IL-10/TNF ratio as compared to BACHD mice. Taken together, our preliminary data propose that the absence of mGluR5 reduce weight gain and visceral adiposity in BACHD mice, along with a decrease in the inflammatory state in the visceral adipose tissue (VAT), which may indicate that mGluR5 may play a role in adiposity modulation.
local.identifier.orcidhttps://orcid.org/0000-0002-3496-6749
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.nature.com/articles/s41598-022-08924-4

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