Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease
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 deleti...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2022-04-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-022-08924-4 |
| _version_ | 1819210102698147840 |
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| author | 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 B. Vieira |
| author_facet | 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 B. Vieira |
| author_sort | Rebeca P. M. Santos |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-23T06:05:51Z |
| format | Article |
| id | doaj.art-11ba8fb0d1b4453b91f7b1ec2705b921 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-12-23T06:05:51Z |
| publishDate | 2022-04-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-11ba8fb0d1b4453b91f7b1ec2705b9212022-12-21T17:57:33ZengNature PortfolioScientific Reports2045-23222022-04-0112111310.1038/s41598-022-08924-4Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s diseaseRebeca P. M. Santos0Roberta Ribeiro1Talita H. Ferreira-Vieira2Rosaria D. Aires3Jessica M. de Souza4Bruna S. Oliveira5Anna Luiza D. Lima6Antônio Carlos P. de Oliveira7Helton J. Reis8Aline S. de Miranda9Erica M. L. Vieira10Fabiola M. Ribeiro11Luciene B. Vieira12Departamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Bioquímica e Imunologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Bioquímica e Imunologia, ICB, Universidade Federal de Minas GeraisDepartamento de Morfologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Morfologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisDepartamento de Bioquímica e Imunologia, ICB, Universidade Federal de Minas GeraisDepartamento de Farmacologia, ICB, Universidade Federal de Minas GeraisAbstract 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.https://doi.org/10.1038/s41598-022-08924-4 |
| spellingShingle | 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 B. Vieira Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease Scientific Reports |
| title | Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease |
| title_full | Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease |
| title_fullStr | Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease |
| title_full_unstemmed | Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease |
| title_short | Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington’s disease |
| title_sort | metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of huntington s disease |
| url | https://doi.org/10.1038/s41598-022-08924-4 |
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