Pulmonary Hypertension in Obese Mice Is Accompanied by a Reduction in PPAR-γ Expression in Pulmonary Artery

dc.contributor.authorGonçalves, Any Elisa de Souza Schmidt
dc.contributor.authorRocha, Guilherme Zweig
dc.contributor.authorMarin, Rodrigo
dc.contributor.authorCamargo, Rafael Ludemann
dc.contributor.authorSantos, Andrey dos
dc.contributor.authorCarmo, Helison do
dc.contributor.authorGuadagnini, Dioze
dc.contributor.authorPetrucci, Orlando
dc.contributor.authorMoysés, Zenaide Providello
dc.contributor.authorSalemi, Vera Maria Cury
dc.contributor.authorOliveira, Alexandre Gabarra [UNESP]
dc.contributor.authorSaad, Mario José Abdalla
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2022-04-29T08:45:55Z
dc.date.available2022-04-29T08:45:55Z
dc.date.issued2021-09-06
dc.description.abstractObesity and insulin resistance (IR) are well-studied risk factors for systemic cardiovascular disease, but their impact on pulmonary hypertension (PH) is not well clarified. This study aims to investigate if diet-induced obesity induces PH and if peroxisome-proliferator-activated receptor (PPAR-γ) and/or endoplasmic reticulum (ER) stress are involved in this process. Mice were maintained on a high-fat diet (HFD) for 4 months, and IR and PH were confirmed. In a separate group, after 4 months of HFD, mice were treated with pioglitazone (PIO) or 4-phenylbutyric acid for the last month. The results demonstrated that HFD for at least 4 months is able to increase pulmonary artery pressure, which is maintained, and this animal model can be used to investigate the link between IR and PH, without changes in ER stress in the pulmonary artery. There was also a reduction in circulating adiponectin and in perivascular adiponectin expression in the pulmonary artery, associated with a reduction in PPAR-γ expression. Treatment with PIO improved IR and PH and reversed the lower expression of adiponectin and PPAR-γ in the pulmonary artery, highlighting this drug as potential benefit for this poorly recognized complication of obesity.en
dc.description.affiliationDepartment of Internal Medicine Faculty of Medicine State University of Campinas
dc.description.affiliationDepartment of Physical Education São Paulo State University (UNESP)
dc.description.affiliationHeart Institute (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
dc.description.affiliationUnespDepartment of Physical Education São Paulo State University (UNESP)
dc.identifierhttp://dx.doi.org/10.3389/fendo.2021.701994
dc.identifier.citationFrontiers in Endocrinology, v. 12.
dc.identifier.doi10.3389/fendo.2021.701994
dc.identifier.issn1664-2392
dc.identifier.scopus2-s2.0-85115231329
dc.identifier.urihttp://hdl.handle.net/11449/231512
dc.language.isoeng
dc.relation.ispartofFrontiers in Endocrinology
dc.sourceScopus
dc.subjecthigh-fat (HF) diet
dc.subjectinsulin resistance
dc.subjectobesity
dc.subjectpioglitazone
dc.subjectPPAR-γ
dc.titlePulmonary Hypertension in Obese Mice Is Accompanied by a Reduction in PPAR-γ Expression in Pulmonary Arteryen
dc.typeArtigo

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