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.

妊娠糖尿病（GDM）是一种妊娠疾病，与d-葡萄糖不耐症和胎儿胎盘血管功能障碍有关。GMD导致胎盘内皮和滋养细胞的线粒体功能障碍。另外，由于线粒体F ₀ F _1的活性降低，GDM与胎盘氧化磷酸化降低有关。-ATP合酶（复合物V）。此现象可能是由于反应性超氧阴离子和一氧化氮的生成量增加。胎盘线粒体的生物发生和线粒体的协同作用可维持细胞稳态，并且是确保有效产生ATP的重要机制，ATP的需求量在妊娠中较高，可确保胎儿的生长发育。干扰GDM中胎盘ATP合酶活性的其他因素包括孕前孕妇肥胖或超重，细胞内pH，miRNA，脂肪酸氧化和胎儿（和“胎盘”）性别。GDM还与母亲和胎儿的高胰岛素血症，脂联素和瘦素的循环水平改变以及细胞外腺苷的积累有关。这里，