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dc.creatorMonteiro, Brenda L.-
dc.creatorSantos, Robson A. S.-
dc.creatorMario, Erica G.-
dc.creatorAraujo, Thiago S.-
dc.creatorSavergnini, Silvia S. Q.-
dc.creatorSantiago, Andrezza F.-
dc.creatorMuzzi, Ruthnea A. L.-
dc.creatorCastro, Isabela C.-
dc.creatorTeixeira, Lilian G.-
dc.creatorBotion, Leida M.-
dc.creatorMarinho, Barbhara M.-
dc.creatorSantos, Sergio H. S.-
dc.creatorPorto, Laura C. J.-
dc.date.accessioned2022-07-04T20:08:42Z-
dc.date.available2022-07-04T20:08:42Z-
dc.date.issued2022-05-
dc.identifier.citationMONTEIRO, B. L. et al. Genetic deletion of Mas receptor in FVB/N mice impairs cardiac use of glucose and lipids. Peptides, [S.I.], v. 151, 170764, May 2022. DOI: https://doi.org/10.1016/j.peptides.2022.170764.pt_BR
dc.identifier.urihttps://doi.org/10.1016/j.peptides.2022.170764pt_BR
dc.identifier.urihttp://repositorio.ufla.br/jspui/handle/1/50462-
dc.description.abstractAngiotensin-(1−7) is a biologically active product of the renin-angiotensin system cascade and exerts inhibitory effects on inflammation, vascular and cellular growth mechanisms signaling through the G protein-coupled Mas receptor. The major purpose of the present study was to investigate the use of glucose and fatty acids by cardiac tissue in Mas knockout mice models. Serum levels of glucose, lipids, and insulin were measured in Mas-deficient and wild-type FVB/N mice. To investigate the cardiac use of lipids, the lipoprotein lipase, the gene expression of peroxisome proliferator-activated receptor alpha; carnitine palmitoyltransferase I and acyl-CoA oxidase were evaluated. To investigate the cardiac use of glucose, the insulin signaling through Akt/GLUT4 pathway, glucose-6-phosphate (G-6-P) and fructose-6-phosphate (F-6-P) glycolytic intermediates, in addition to ATP, lactate and the glycogen content were measured. Despite normal body weight, cholesterol and insulin, Mas-Knockout mice presented hyperglycemia and hypertriglyceridemia, impaired insulin signaling, through reduced phosphorylation of AKT and decreased translocation of GLUT4 in response to insulin, with subsequent decrease of the cardiac G-6-P and F-6-P. Lactate production and glycogen content were not altered in Mas-KO hearts. Mas-KO presented reduced cardiac lipoprotein lipase activity and decreased translocation of CD36 in response to insulin. The expression of peroxisome proliferator-activated receptor alpha and carnitine palmitoyltransferase I genes were lower in Mas-KO animals compared to wild-type animals. The ATP content of Mas-KO hearts was smaller than in wild-type. The present results suggest that genetic deletion of Mas produced a devastating effect on cardiac use of glucose and lipids, leading to lower energy efficiency in the heart.pt_BR
dc.languageenpt_BR
dc.publisherElsevierpt_BR
dc.rightsrestrictAccesspt_BR
dc.sourcePeptidespt_BR
dc.subjectRenin-angiotensin systempt_BR
dc.subjectHeart metabolismpt_BR
dc.subjectInsulin signalingpt_BR
dc.subjectGlucosept_BR
dc.subjectFatty acidspt_BR
dc.subjectAngiotensin-(1-7)pt_BR
dc.subjectSistema renina-angiotensinapt_BR
dc.subjectMetabolismo cardíacopt_BR
dc.subjectSinalização da insulinapt_BR
dc.subjectGlicosept_BR
dc.subjectÁcidos graxospt_BR
dc.subjectAngiotensina(1-7)pt_BR
dc.titleGenetic deletion of Mas receptor in FVB/N mice impairs cardiac use of glucose and lipidspt_BR
dc.typeArtigopt_BR
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