Nutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, Washington.
Laboratory of Perinatal Kinesioepigenetics, Department of Obstetrics, Gynecology & Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland.
Am J Physiol Endocrinol Metab. 2022 Jun 1;322(6):E467-E479. doi: 10.1152/ajpendo.00023.2022. Epub 2022 Apr 11.
Maternal exercise (ME) protects against adverse effects of maternal obesity (MO) on fetal development. As a cytokine stimulated by exercise, apelin (APN) is elevated due to ME, but its roles in mediating the effects of ME on placental development remain to be defined. Two studies were conducted. In the first study, 18 female mice were assigned to control (CON), obesogenic diet (OB), or OB with exercise (OB/Ex) groups ( = 6); in the second study, the same number of female mice were assigned to three groups; CON with PBS injection (CD/PBS), OB/PBS, or OB with apelin injection (OB/APN). In the exercise study, daily treadmill exercise during pregnancy significantly elevated the expression of PR domain 16 (PRDM16; < 0.001), which correlated with enhanced oxidative metabolism and mitochondrial biogenesis in the placenta ( < 0.05). More importantly, these changes were partially mirrored in the apelin study. Apelin administration upregulated PRDM16 protein level ( < 0.001), mitochondrial biogenesis ( < 0.05), placental nutrient transporter expression ( < 0.001), and placental vascularization ( < 0.01), which were impaired due to MO ( < 0.05). In summary, MO impairs oxidative phosphorylation in the placenta, which is improved by ME; apelin administration partially mimics the beneficial effects of exercise on improving placental function, which prevents placental dysfunction due to MO. Maternal exercise prevents metabolic disorders of mothers and offspring induced by high-fat diet. Exercise intervention enhances PRDM16 activation, oxidative metabolism, and vascularization of placenta, which are inhibited due to maternal obesity. Similar to maternal exercise, apelin administration improves placental function of obese dams.
母体运动（ME）可预防母体肥胖（MO）对胎儿发育的不良影响。作为一种由运动刺激的细胞因子，apelin（APN）因 ME 而升高，但它在介导 ME 对胎盘发育的影响方面的作用仍有待确定。进行了两项研究。在第一项研究中，将 18 只雌性小鼠分配到对照组（CON）、肥胖诱导饮食组（OB）或肥胖诱导饮食+运动组（OB/Ex）（每组 6 只）；在第二项研究中，将相同数量的雌性小鼠分配到三组：CON+PBS 注射组（CD/PBS）、OB+PBS 注射组或 OB+apelin 注射组（OB/APN）。在运动研究中，怀孕期间每天进行跑步机运动显著提高了 PR 结构域 16（PRDM16；<0.001）的表达，这与胎盘氧化代谢和线粒体生物发生增强相关（<0.05）。更重要的是，这些变化在 apelin 研究中部分得到了反映。apelin 给药上调了 PRDM16 蛋白水平（<0.001）、线粒体生物发生（<0.05）、胎盘营养转运蛋白表达（<0.001）和胎盘血管生成（<0.01），这些变化因 MO 而受损（<0.05）。总之，MO 损害了胎盘的氧化磷酸化，而 ME 则改善了这种损害；apelin 给药部分模拟了运动改善胎盘功能的有益作用，从而防止了 MO 引起的胎盘功能障碍。母体运动可预防高脂肪饮食引起的母亲和后代的代谢紊乱。运动干预增强了胎盘的 PRDM16 激活、氧化代谢和血管生成，而这些因母体肥胖而受到抑制。与母体运动类似，apelin 给药改善了肥胖母鼠的胎盘功能。
