Author:
Santos Rebeca P. M.,Ribeiro Roberta,Ferreira-Vieira Talita H.,Aires Rosaria D.,de Souza Jessica M.,Oliveira Bruna S.,Lima Anna Luiza D.,de Oliveira Antônio Carlos P.,Reis Helton J.,de Miranda Aline S.,Vieira Erica M. L.,Ribeiro Fabiola M.,Vieira Luciene B.
Abstract
AbstractObesity 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.
Funder
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Pró-Reitoria de Pesquisa, Universidade Federal de Minas Gerais
Publisher
Springer Science and Business Media LLC
Cited by
3 articles.
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