Investigating mitochondrial dysfunction in gestational diabetes mellitus and elucidating if BMI is a causative mediator

dc.check.date2021-05-21
dc.check.infoAccess to this article is restricted until 12 months after publication by request of the publisher.en
dc.contributor.authorMcElwain, Colm
dc.contributor.authorMcCarthy, Cathal M.
dc.contributor.funderHealth Research Boarden
dc.date.accessioned2020-08-04T09:45:04Z
dc.date.available2020-08-04T09:45:04Z
dc.date.issued2020-05-21
dc.date.updated2020-08-04T09:37:02Z
dc.description.abstractObjective: Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance which is diagnosed during pregnancy and poses considerable health risks for mother and child. Maternal body mass index (BMI) correlates with GDM diagnosis and the pathophysiology of this link may be explained through oxidative stress and mitochondrial dysfunction. In this study we investigate if mitochondrial dysfunction is evident in GDM by measuring cell free mitochondrial DNA concentration and determine if a potential relationship exists between maternal mitochondrial function and GDM diagnosis. Study design: Plasma samples were taken at 20 weeks' gestation from women who subsequently developed GDM (n = 44) and matched with women with uncomplicated pregnancies (n = 85) as controls. Control group 1 was matched by maternal age and BMI (n = 41) to GDM cases, while control group 2 was matched by maternal age alone (n = 44). Prediction potential was determined by binary regression analysis. Statistical analysis was performed on SPSS Statistics v25. Results: Binary regression analysis showed a statistically significant association between mtDNA concentration and GDM diagnosis (p = 0.032) in GDM cases versus control group 2, indicating that GDM patients have higher circulating mtDNA concentrations relative to healthy control patients. The lack of statistical significance in control group 1 suggests that BMI may be linked to mitochondrial function in GDM patients. Conclusion: These results demonstrate a potential pathogenic role for mitochondrial dysfunction in GDM, with BMI presenting as a likely physiological mediator.en
dc.description.sponsorshipHealth Research Board (Project Code: HRB-EIA-2017-021)en
dc.description.statusPeer revieweden
dc.description.versionAccepted Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationMcElwain, C. and McCarthy, C. M. (2020) 'Investigating mitochondrial dysfunction in gestational diabetes mellitus and elucidating if BMI is a causative mediator', European Journal of Obstetrics and Gynecology and Reproductive Biology, 251, pp. 60-65. doi: 10.1016/j.ejogrb.2020.04.037en
dc.identifier.doi10.1016/j.ejogrb.2020.04.037en
dc.identifier.endpage65en
dc.identifier.issn0301-2115
dc.identifier.journaltitleEuropean Journal of Obstetrics and Gynecology and Reproductive Biologyen
dc.identifier.startpage60en
dc.identifier.urihttps://hdl.handle.net/10468/10351
dc.identifier.volume251en
dc.language.isoenen
dc.publisherElsevier B.V.en
dc.rights© 2020, Elsevier B.V. All rights reserved. This manuscript version is made available under the CC BY-NC-ND 4.0 license.en
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.subjectAdiposityen
dc.subjectGDMen
dc.subjectInsulin resistanceen
dc.subjectMitochondriaen
dc.titleInvestigating mitochondrial dysfunction in gestational diabetes mellitus and elucidating if BMI is a causative mediatoren
dc.typeArticle (peer-reviewed)en
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