Publicação:
Mitochondrial dysfunction in the fetoplacental unit in gestational diabetes mellitus

dc.contributor.authorSobrevia, Luis
dc.contributor.authorValero, Paola
dc.contributor.authorGrismaldo, Adriana
dc.contributor.authorVillalobos-Labra, Roberto
dc.contributor.authorPardo, Fabián
dc.contributor.authorSubiabre, Mario
dc.contributor.authorArmstrong, Gael
dc.contributor.authorToledo, Fernando
dc.contributor.authorVega, Sofía [UNESP]
dc.contributor.authorCornejo, Marcelo
dc.contributor.authorFuentes, Gonzalo
dc.contributor.authorMarín, Reinaldo
dc.contributor.institutionPontificia Universidad Católica de Chile
dc.contributor.institutionUniversidad de Valparaíso
dc.contributor.institutionPontificia Universidad Javeriana
dc.contributor.institutionUniversity of Alberta
dc.contributor.institutionUniversidad del Bío-Bío
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidad de Talca
dc.contributor.institutionVenezuelan Institute for Scientific Research (IVIC)
dc.contributor.institutionUniversidad de Sevilla
dc.contributor.institutionUniversity of Queensland
dc.date.accessioned2020-12-12T02:22:05Z
dc.date.available2020-12-12T02:22:05Z
dc.date.issued2020-12-01
dc.description.abstractGestational diabetes mellitus (GDM) is a disease of pregnancy that is associated with D-glucose intolerance and foeto-placental vascular dysfunction. GMD causes mitochondrial dysfunction in the placental endothelium and trophoblast. Additionally, GDM is associated with reduced placental oxidative phosphorylation due to diminished activity of the mitochondrial F0F1-ATP synthase (complex V). This phenomenon may result from a higher generation of reactive superoxide anion and nitric oxide. Placental mitochondrial biogenesis and mitophagy work in concert to maintain cell homeostasis and are vital mechanisms securing the efficient generation of ATP, whose demand is higher in pregnancy, ensuring foetal growth and development. Additional factors disturbing placental ATP synthase activity in GDM include pre-gestational maternal obesity or overweight, intracellular pH, miRNAs, fatty acid oxidation, and foetal (and ‘placental’) sex. GDM is also associated with maternal and foetal hyperinsulinaemia, altered circulating levels of adiponectin and leptin, and the accumulation of extracellular adenosine. Here, we reviewed the potential interplay between these molecules or metabolic conditions on the mechanisms of mitochondrial dysfunction in the foeto-placental unit in GDM pregnancies.en
dc.description.affiliationCellular and Molecular Physiology Laboratory (CMPL) Department of Obstetrics Division of Obstetrics and Gynaecology School of Medicine Faculty of Medicine Pontificia Universidad Católica de Chile
dc.description.affiliationFaculty of Science Faculty of Engineering Faculty of Medicine Universidad de Valparaíso
dc.description.affiliationFaculty of Sciences Department of Nutrition and Biochemistry Pontificia Universidad Javeriana
dc.description.affiliationDepartment of Obstetrics and Gynaecology Heritage Medical Research Centre (HMRC) University of Alberta
dc.description.affiliationMetabolic Diseases Research Laboratory Interdisciplinary Centre of Territorial Health Research (CIISTe) Biomedical Research Center (CIB) San Felipe Campus School of Medicine Faculty of Medicine Universidad de Valparaíso
dc.description.affiliationDepartment of Basic Sciences Faculty of Sciences Universidad del Bío-Bío
dc.description.affiliationDepartment of Gynaecology and Obstetrics Botucatu Medical School (FMB) São Paulo State University (UNESP)
dc.description.affiliationFaculty of Health Sciences Universidad de Talca
dc.description.affiliationLaboratory of Cell Bioenergetics Center for Biophysics and Biochemistry (CBB) Venezuelan Institute for Scientific Research (IVIC), AP 21827
dc.description.affiliationDepartment of Physiology Faculty of Pharmacy Universidad de Sevilla
dc.description.affiliationUniversity of Queensland Centre for Clinical Research (UQCCR) Faculty of Medicine and Biomedical Sciences University of Queensland
dc.description.affiliationUnespDepartment of Gynaecology and Obstetrics Botucatu Medical School (FMB) São Paulo State University (UNESP)
dc.description.sponsorshipFondo Nacional de Desarrollo Científico y Tecnológico
dc.description.sponsorshipFondo Nacional de Ciencia Tecnología e Innovación
dc.description.sponsorshipIdFondo Nacional de Desarrollo Científico y Tecnológico: 1190316
dc.description.sponsorshipIdFondo Nacional de Ciencia Tecnología e Innovación: F-2005000222
dc.identifierhttp://dx.doi.org/10.1016/j.bbadis.2020.165948
dc.identifier.citationBiochimica et Biophysica Acta - Molecular Basis of Disease, v. 1866, n. 12, 2020.
dc.identifier.doi10.1016/j.bbadis.2020.165948
dc.identifier.issn1879-260X
dc.identifier.issn0925-4439
dc.identifier.scopus2-s2.0-85090423936
dc.identifier.urihttp://hdl.handle.net/11449/201019
dc.language.isoeng
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Basis of Disease
dc.sourceScopus
dc.subjectAdenosine
dc.subjectEndothelium
dc.subjectGestational diabetes
dc.subjectHuman
dc.subjectInsulin
dc.subjectMitochondria
dc.subjectPlacenta
dc.titleMitochondrial dysfunction in the fetoplacental unit in gestational diabetes mellitusen
dc.typeResenha
dspace.entity.typePublication
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt
unesp.departmentGinecologia e Obstetrícia - FMBpt

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