Detalhes bibliográficos
Título da fonte: Repositório Institucional da UFMG
id UFMG_98c0d2ce291946f6fa498ca69148b0e7
oai_identifier_str oai:repositorio.ufmg.br:1843/60917
network_acronym_str UFMG
network_name_str Repositório Institucional da UFMG
repository_id_str
reponame_str Repositório Institucional da UFMG
instacron_str UFMG
institution Universidade Federal de Minas Gerais (UFMG)
instname_str Universidade Federal de Minas Gerais (UFMG)
spelling 2023-11-13T22:35:49Z2023-11-13T22:35:49Z2022-09-141255112https://doi.org/10.1186/s43066-022-00216-w2090-6226http://hdl.handle.net/1843/60917http://orcid.org/0000-0002-7788-5447CNPq - Conselho Nacional de Desenvolvimento Científico e TecnológicoFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas GeraisCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorBackground Telmisartan is a non-peptide angiotensin II receptor antagonist which acts by ACE/AngII/AT1 axis blockade (ARB). In the last years increasing evidence of its metabolic benefits pointed out this drug as the most promising ARB for nonalcoholic fatty liver disease (NAFLD) treatment. The aim of the present study was to investigate the Telmisartan effect on treating NAFLD in mice fed with a high-fat diet evaluating liver gene modulation. Twenty-four male mice were divided into four groups and fed for 60 days with a standard diet (ST), standard diet plus TEL (ST+TEL 5 mg/kg/day by gavage for 4 weeks), high-fat diet (HFD), or high-fat diet plus TEL (HFD+TEL 5 mg/kg/day by gavage for 4 weeks). Body weight, lipid profile, insulin, alanine transaminase, and aspartate aminotransferase were evaluated. Liver histology was analyzed. US imaging was performed to access liver dimension and echogenicity and also epididymal fat pad thickness. The expression of proinflammatory resistin/TRL4/MYD88 pathway was analyzed. Results The main findings showed that TEL reduced the resistin, TRL4, and Myd88 liver expression in the HFD + TEL group when compared to the obese control group (HFD). Decreased hepatic steatosis in the HFD + TEL group demonstrated by US measurements of the liver longitudinal axis and echogenicity were observed. In addition, TEL reduced epididymal adipose pad thickness, body weight, transaminases, and improved glucose tolerance test and HDL cholesterol. Conclusions We observed that Telmisartan treatment improved metabolism, decreasing NAFLD.engUniversidade Federal de Minas GeraisUFMGBrasilICA - INSTITUTO DE CIÊNCIAS AGRÁRIASEgyptian Liver JournalObesidadeFígadoRenin-angiotensin systemObesityAngiotensin-(1–7)Non-alcoholic fatty liver diseaseAngiotensin II type 1 receptor (AT1) blockade by Telmisartan attenuates hepatic steatosis in high-fat fed mice reducing Resistin, TRL4, and Myd88 expressioninfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttps://eglj.springeropen.com/articles/10.1186/s43066-022-00216-w#rightslinkLuciana Mendes Araújo BorémSergio Henrique Sousa SantosDaniela Fernanda de FreitasAmanda Souto MachadoAlanna Fernandes ParaisoBruna Viana CaldasJoão Felício Rodrigues NetoJuliana Pinto LimaAndré Luiz Senna GuimarãesAlfredo Mauricio Batista de Paulaapplication/pdfinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMGLICENSELicense.txtLicense.txttext/plain; charset=utf-82042https://repositorio.ufmg.br/bitstream/1843/60917/1/License.txtfa505098d172de0bc8864fc1287ffe22MD51ORIGINALAngiotensin II type 1 receptor (AT1) blockade by Telmisartan attenuates hepatic steatosis in high-fat fed mice reducing Resistin, TRL4, and Myd88 expression.pdfAngiotensin II type 1 receptor (AT1) blockade by Telmisartan attenuates hepatic steatosis in high-fat fed mice reducing Resistin, TRL4, and Myd88 expression.pdfapplication/pdf1351092https://repositorio.ufmg.br/bitstream/1843/60917/2/Angiotensin%20II%20type%201%20receptor%20%28AT1%29%20blockade%20by%20Telmisartan%20attenuates%20hepatic%20steatosis%20in%20high-fat%20fed%20mice%20reducing%20Resistin%2c%20TRL4%2c%20and%20Myd88%20expression.pdfec5f8be6818aa6a5310921d70fb8a0ffMD521843/609172023-11-13 19:35:49.883oai:repositorio.ufmg.br:1843/60917Repositório InstitucionalPUBhttps://repositorio.ufmg.br/oaiopendoar:2023-11-13T22:35:49Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false
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