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

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dc.contributor.author McElwain, Colm
dc.contributor.author McCarthy, Cathal M.
dc.date.accessioned 2020-08-04T09:45:04Z
dc.date.available 2020-08-04T09:45:04Z
dc.date.issued 2020-05-21
dc.identifier.citation McElwain, 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.2020.04.037 en
dc.identifier.volume 251 en
dc.identifier.startpage 60 en
dc.identifier.endpage 65 en
dc.identifier.issn 0301-2115
dc.identifier.uri http://hdl.handle.net/10468/10351
dc.identifier.doi 10.1016/j.ejogrb.2020.04.037 en
dc.description.abstract Objective: 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.sponsorship Health Research Board (Project Code: HRB-EIA-2017-021) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Elsevier 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.uri https://creativecommons.org/licenses/by-nc-nd/4.0/ en
dc.subject Adiposity en
dc.subject GDM en
dc.subject Insulin resistance en
dc.subject Mitochondria en
dc.title Investigating mitochondrial dysfunction in gestational diabetes mellitus and elucidating if BMI is a causative mediator en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Cathal Mccarthy, Pharmacology & Therapeutics, University College Cork, Cork, Ireland. +353-21-490-3000 Email: cmccarthy@ucc.ie en
dc.internal.availability Full text available en
dc.check.info Access to this article is restricted until 12 months after publication by request of the publisher. en
dc.check.date 2021-05-21
dc.date.updated 2020-08-04T09:37:02Z
dc.description.version Accepted Version en
dc.internal.rssid 517084855
dc.contributor.funder Health Research Board en
dc.description.status Peer reviewed en
dc.identifier.journaltitle European Journal of Obstetrics and Gynecology and Reproductive Biology en
dc.internal.copyrightchecked Yes
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress cmccarthy@ucc.ie en


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© 2020, Elsevier B.V. All rights reserved. This manuscript version is made available under the CC BY-NC-ND 4.0 license. Except where otherwise noted, this item's license is described as © 2020, Elsevier B.V. All rights reserved. This manuscript version is made available under the CC BY-NC-ND 4.0 license.
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