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Exercise performed during pregnancy positively modulates liver metabolism and promotes mitochondrial biogenesis of female offspring in a rat model of diet-induced gestational diabetes

2022-11-01Journal article Restricted access
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dc.contributor.authorStevanović-Silva, Jelena
dc.contributor.authorBeleza, Jorge
dc.contributor.authorCoxito, Pedro
dc.contributor.authorRocha, Hugo
dc.contributor.authorGaspar, Tiago Bordeira
dc.contributor.authorGärtner, Fátima
dc.contributor.authorCorreia, Rossana
dc.contributor.authorFernandes, Rui
dc.contributor.authorOliveira, Paulo J.
dc.contributor.authorAscensão, António
dc.contributor.authorMagalhães, José
dc.date.accessioned2023-03-20T14:55:59Z
dc.date.available2023-03-20T14:55:59Z
dc.date.issued2022-11-01
dc.description.abstractGestational diabetes mellitus (GDM) is associated with a high-risk for metabolic complications in offspring. However, exercise is recognized as a non-pharmacological strategy against metabolic disorders and is recommended in GDM treatment. This study aimed to investigate whether gestational exercise (GE) could modulate maternal high-fat high-sucrose (HFHS) diet-related hepatic metabolic and mitochondrial outcomes in female offspring of mothers with HFHS-induced GDM. Female Sprague-Dawley rats were fed with control or HFHS diet and kept sedentary or submitted to GE. Their female offspring were fed with control diet and kept sedentary. Hepatic lipid accumulation, lipid metabolism regulators, mitochondrial biogenesis and dynamics markers, and microRNAs associated to the regulation of these markers were evaluated. Female offspring of GDM mothers showed increased body weight at early age, whereas GE prevented this effect of maternal HFHS-feeding and reduced hepatic lipid accumulation. GE stimulated hepatic mRNA transcription and protein expression of mitochondrial biogenesis markers (peroxisome proliferator-activated receptor-gamma co-activator-1alpha and mitochondrial transcription factor A) and mRNA transcription of mitochondrial dynamics markers (mitofusin-1, mitofusin-2, and dynamin-related protein-1) that were altered by maternal GDM, while mitochondrial dynamics markers protein expression was not affected by maternal diet/GE except for optic atrophy-1. MicroRNAs associated with these processes (miR-122, miR-34a, miR-130b, miR-494), and the expression of auto/mitophagy- and apoptosis-related proteins were not substantially influenced by altered intrauterine environment. Our findings suggest that GE is an important regulator of the intrauterine environment positively affecting liver metabolism and promoting liver mitochondrial biogenesis in female offspring despite eventual effects of maternal HFHS-feeding and related GDM.pt_PT
dc.description.abstractHighlights: Maternal lifestyle can affect hepatic metabolic status of their female offspring; Female offspring hepatic metabolism is affected by maternal high-fat/sucrose diet; Gestational exercise mitigated maternal diet-related harmful outcomes on offspring liver; Gestational exercise is an important regulator of offspring mitochondrial biogenesis and dynamics; Exercise programs should be encouraged in clinical counseling during pregnancy.pt_PT
dc.description.sponsorshipThis work was supported by the EU's Horizon 2020 Research and Innovation program under the Marie Skłodowska-Curie Actions (No.722619, FOIE GRAS; No.734719, mtFOIE GRAS) and by the Por tuguese Foundation for Science and Technology (FCT) (FCT/UID/DTP/00617/2020-base; POCI-01-0145-FEDER-016690-PTDC/DTP-DES/7087/2014; POCI-01-0145-FEDER-016657-PTDC/DTP-DES/1082/2014), to JB (SFRH/BD/129645/2017).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationBiochim Biophys Acta Mol Basis Dis. 2022 Nov 1;1868(11):166526. doi: 10.1016/j.bbadis.2022.166526. Epub 2022 Aug 20.pt_PT
dc.identifier.doi10.1016/j.bbadis.2022.166526pt_PT
dc.identifier.issn0925-4439
dc.identifier.urihttp://hdl.handle.net/10400.18/8575
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationBioenergetic Remodeling in the Pathophysiology and Treatment of Non-Alcoholic Fatty Liver Disease
dc.relationResearch Center in Physical Activity , Health and Leisure
dc.relationExercising obesity - the role of exercise against endoplasmic reticulum stress in obesity-induced liver disease
dc.relationAre cardiac and brain epigenetic modifications induced by physical exercise transgenerationally inherited Focus on mitochondrial-related adaptations.
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0925443922001971?via%3Dihubpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectFetal Programmingpt_PT
dc.subjectGestational Exercisept_PT
dc.subjectPhysical Exercisept_PT
dc.subjectPregnancypt_PT
dc.subjectDoenças Genéticaspt_PT
dc.titleExercise performed during pregnancy positively modulates liver metabolism and promotes mitochondrial biogenesis of female offspring in a rat model of diet-induced gestational diabetespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleBioenergetic Remodeling in the Pathophysiology and Treatment of Non-Alcoholic Fatty Liver Disease
oaire.awardTitleResearch Center in Physical Activity , Health and Leisure
oaire.awardTitleExercising obesity - the role of exercise against endoplasmic reticulum stress in obesity-induced liver disease
oaire.awardTitleAre cardiac and brain epigenetic modifications induced by physical exercise transgenerationally inherited Focus on mitochondrial-related adaptations.
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/722619/EU
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDB%2F00617%2F2020/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FDTP-DES%2F7087%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/9471 - RIDTI/PTDC%2FDTP-DES%2F1082%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F129645%2F2017/PT
oaire.citation.issue11pt_PT
oaire.citation.startPage166526pt_PT
oaire.citation.titleBiochimica et Biophysica Acta (BBA) - Molecular Basis of Diseasept_PT
oaire.citation.volume1868pt_PT
oaire.fundingStreamH2020
oaire.fundingStream6817 - DCRRNI ID
oaire.fundingStream9471 - RIDTI
oaire.fundingStream9471 - RIDTI
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameEuropean Commission
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.embargofctAcesso de acordo com política editorial da revista.pt_PT
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication76692f35-e5b4-49db-8bc2-b413dafc19bc
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