Genetic deletion of the angiotensin-(1–7) receptor Mas leads to alterations in gut villi length modulating TLR4/PI3K/AKT and produces microbiome dysbiosis

Página do item simplificado
dc.creatorLuis Paulo Oliveira
dc.creatorVictor Hugo Dantas Guimarães
dc.creatorJanaína Ribeiro Oliveira
dc.creatorAndré Luiz Sena Guimarães
dc.creatorAlfredo Maurício Batista de Paula
dc.creatorMichael Bader
dc.creatorRobson Augusto Souza dos Santos
dc.creatorSergio Henrique Sousa Santos
dc.date.accessioned2022-09-05T13:20:58Z
dc.date.accessioned2025-09-08T23:53:57Z
dc.date.available2022-09-05T13:20:58Z
dc.date.issued2020-08
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
dc.identifier.doihttps://doi.org/10.1016/j.npep.2020.102056
dc.identifier.issn1532-2785
dc.identifier.urihttps://hdl.handle.net/1843/44900
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofNeuropeptides
dc.rightsAcesso Restrito
dc.subjectSistema renina-angiotensina
dc.subjectIntestino delgado
dc.subjectInflamação
dc.titleGenetic deletion of the angiotensin-(1–7) receptor Mas leads to alterations in gut villi length modulating TLR4/PI3K/AKT and produces microbiome dysbiosis
dc.typeArtigo de periódico
local.citation.spage102056
local.citation.volume18
local.description.resumoRenin-Angiotensin System (RAS) is an important peptide cascade involved in physiological processes. RAS homeostasis disruption produces several cardiovascular and metabolic disorders, such as arterial hypertension, atherosclerosis, acute myocardial infarct, obesity, diabetes, metabolic syndrome and increases gastrointestinal tract (GIT) cell proliferation. Angiotensin (Ang)-(1–7) peptide is the main RAS counter-regulatory axis effector. It is formed from ACE2 enzyme and acts mainly through Mas receptor (MasR). In this context, the aim of the present study was to evaluate alterations in small intestine morphology and intestinal microbiota composition in MasR knockout C57BL/6 mice. We analyzed glucose tolerance; insulin sensitivity and blood collected for biochemical parameters as well as small intestine tissues samples for immunohistochemistry. mRNA and bacteria gDNA expression evaluation. mRNA expression was evaluated by qRT-PCR for TLR4, PI3K and AKT. The main results showed that Mas-R-knockout mice presented lower body weight. MasR-knockout mice also presented increased fasted blood glucose and total cholesterol with reduced HDL, lower glucose tolerance and impaired insulin sensitivity. Increased intestinal mucosa length, increased intestinal villi, reduced Lieberkühn crypt depth. The increased expression of cell proliferation markers Ki-67 and Cyclin D1 and increased TLR4, PI3K and AKT expressions were observed with augmented Bacteroidetes and decreased amount of Firmicutes. That results suggests that MasR deletion generated changes in intestinal microbiota, possibly due to a lower neutral amino acids absorption followed by a compensatory increase in intestinal villi length associated with disbiosis and LPS overproduction that ultimately lead to proliferation and cell inflammation.
local.publisher.countryBrasil
local.publisher.departmentICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/pii/S014341792030069X

Arquivos

Licença do pacote

Agora exibindo 1 - 1 de 1
Imagem de Miniatura
Nome:
License.txt
Tamanho:
1.99 KB
Formato:
Plain Text
Descrição:
Baixar

Coleções

Artigo de Periódico

Logo UFMG