Maternal obesity modulates both the renin–angiotensin system in mice dams and fetal adiposity

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dc.creatorGabriela Cavazza Cerri
dc.creatorDaisy Motta Santos
dc.creatorJoão Marcus Oliveira Andrade
dc.creatorLuiz Fernando de Rezende
dc.creatorRobson Augusto Souza dos Santos
dc.creatorSergio Henrique Sousa Santos
dc.date.accessioned2022-08-30T15:08:44Z
dc.date.accessioned2025-09-09T00:18:52Z
dc.date.available2022-08-30T15:08:44Z
dc.date.issued2020-10
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.jnutbio.2020.108413
dc.identifier.issn1873-4847
dc.identifier.urihttps://hdl.handle.net/1843/44725
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofThe Journal of Nutritional Biochemistry
dc.rightsAcesso Restrito
dc.subjectObesidade
dc.subjectAngiotensina
dc.subjectSistema renina-angiotensina
dc.subjectGravidez
dc.subjectTecido adiposo
dc.titleMaternal obesity modulates both the renin–angiotensin system in mice dams and fetal adiposity
dc.typeArtigo de periódico
local.citation.spage108413
local.citation.volume84
local.description.resumoObesity is a chronic multifactorial disease and is currently a public health problem. Maternal obesity during pregnancy is more dangerous as it impairs the health of the mother and future generations. Obesity leads to several metabolic disorders. Since white adipose tissue is an endocrine tissue, obesity often leads to disordered secretion of inflammatory, glycemic, lipid and renin–angiotensin system (RAS) components. The RAS represents a link between obesity and its metabolic consequences. Therefore, our goal was to evaluate the possible changes caused by a high-fat diet in RAS-related receptor expression in the uterus and placenta of pregnant mice and determine the underlying effects of these changes in the fetuses’ body composition. Breeding groups were formed after obesity induction by high-fat (HF) diet. Dams and fetuses were euthanized on the 19th day of the gestational period. The HF diet effectively induced obesity, glucose intolerance and insulin resistance in mice. Fetuses born from HF dams showed increased body weight and adiposity. Both results were accompanied by increased AT1R expression in placenta and uterus together with increased angiotensin-converting enzyme expression in the uterus and a decreased expression of MAS1 in placenta of HF dams. These results suggest a link between RAS, maternal obesity induced by HF diet and the fetuses’ body adiposity. This new path now can be more thoroughly explored.
local.publisher.countryBrasil
local.publisher.departmentICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/pii/S0955286320304459

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