Mitochondrial dysfunction in the fetoplacental unit in gestational diabetes mellitus

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1866

Review

Sobrevia, Luis^1,10,11  Valero, Paola^1,2  Grismaldo, Adriana^1,3  Villalobos-Labra, Roberto⁴  Pardo, Fabian^1,5  Subiabre, Mario¹  Armstrong, Gael¹  Toledo, Fernando^1,6  Vega, Sofia^1,7  Cornejo, Marcelo^1,8  Fuentes, Gonzalo^1,8  Marin, Reinaldo⁹ 

[1] Pontificia Univ Catolica Chile, Fac Med, Sch Med, Cellular & Mol Physiol Lab CMPL,Dept Obstet,Div O, POB 114-D, Santiago 8330024, Chile

[2] Univ Valparaiso, Fac Sci, Fac Engn, Fac Med, Vina Del Mar 2520000, Chile

[3] Pontificia Univ Javeriana, Fac Sci, Dept Nutr & Biochem, Bogota, Colombia

[4] Univ Alberta, Heritage Med Res Ctr HMRC, Dept Obstet & Gynaecol, Edmonton, AB T6G 2S2, Canada

[5] Univ Valparaiso, Fac Med, Interdisciplinary Ctr Terr Hlth Res CIISTe, Metab Dis Res Lab,Biomed Res Ctr CIB,Sch Med, San Felipe Campus, San Felipe 2172972, Chile

[6] Univ Bio Bio, Fac Sci, Dept Basic Sci, Chillan 3780000, Chile

[7] Sao Paulo State Univ UNESP, Botucatu Med Sch FMB, Dept Gynaecol & Obstet, BR-18618687 Sao Paulo, Brazil

[8] Univ Talca, Fac Hlth Sci, Talca 3460000, Chile

[9] Venezuelan Inst Sci Res IVIC, Ctr Biophys & Biochem CBB, Lab Cell Bioenerget, AP 21827, Caracas 1020A, Venezuela

[10] Univ Seville, Fac Pharm, Dept Physiol, E-41012 Seville, Spain

[11] Univ Queensland, Univ Queensland Ctr Clin Res UQCCR, Fac Med & Biomed Sci, Herston, Qld 4029, Australia

关键词: Gestational diabetes;    Placenta;    Mitochondria;    Insulin;    Adenosine;    Endothelium;    Human;   

DOI  :  10.1016/j.bbadis.2020.165948

来源: Elsevier

【 摘 要 】

Gestational 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.

【 授权许可】

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