Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/60288
Type: Artigo de Periódico
Title: Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease.
Authors: Rebeca P. M. Santos
Roberta Ribeiro
Talita H. Ferreira-Vieira
Rosaria D. Aires
Jessica M. de Souza
Bruna S. Oliveira
Anna Luiza D. Lima
Antônio Carlos P. de Oliveira
Helton J. Reis
Aline S. de Miranda
Erica M. L. Vieira
Fabiola M. Ribeiro
Luciene Bruno Vieira
Abstract: Obesity 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.
Subject: Receptores de Glutamato Metabotrópico 5
Obesidade
Doença de Huntington
Camundongos knockout
language: eng
metadata.dc.publisher.country: Brasil
Publisher: Universidade Federal de Minas Gerais
Publisher Initials: UFMG
metadata.dc.publisher.department: ICB - DEPARTAMENTO DE FARMACOLOGIA
Rights: Acesso Aberto
metadata.dc.identifier.doi: https://doi.org/10.1038/s41598-022-08924-4
URI: http://hdl.handle.net/1843/60288
Issue Date: 2022
metadata.dc.url.externa: https://www.nature.com/articles/s41598-022-08924-4
metadata.dc.relation.ispartof: Scientific Reports
Appears in Collections:Artigo de Periódico



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