Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/44900
Type: Artigo de Periódico
Title: Genetic deletion of the angiotensin-(1–7) receptor Mas leads to alterations in gut villi length modulating TLR4/PI3K/AKT and produces microbiome dysbiosis
Authors: Luis Paulo Oliveira
Victor Hugo Dantas Guimarães
Janaína Ribeiro Oliveira
André Luiz Sena Guimarães
Alfredo Maurício Batista de Paula
Michael Bader
Robson Augusto Souza dos Santos
Sergio Henrique Sousa Santos
Abstract: Renin-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.
Subject: Sistema renina-angiotensina
Intestino delgado
Inflamação
language: eng
metadata.dc.publisher.country: Brasil
Publisher: Universidade Federal de Minas Gerais
Publisher Initials: UFMG
metadata.dc.publisher.department: ICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS
Rights: Acesso Restrito
metadata.dc.identifier.doi: https://doi.org/10.1016/j.npep.2020.102056
URI: http://hdl.handle.net/1843/44900
Issue Date: Aug-2020
metadata.dc.url.externa: https://www.sciencedirect.com/science/article/pii/S014341792030069X
metadata.dc.relation.ispartof: Neuropeptides
Appears in Collections:Artigo de Periódico

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.