Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis
文献类型： 外文期刊
作者： Son, Jun Seok 1 ; Chae, Song Ah 1 ; Wang, Hongyang 2 ; Chen, Yanting 1 ; Iniguez, Alejandro Bravo 4 ; de Avila, Jea 1 ;
作者机构： 1.Washington State Univ, Dept Anim Sci, Nutrigen & Growth Biol Lab, Pullman, WA 99164 USA
2.Shanghai Acad Agr Sci, Inst Anim Husb & Vet Sci, Shanghai, Peoples R China
3.Washington State Univ, Sch Mol Biosci, Pullman, WA 99164 USA
4.Washington State Univ, Sch Food Sci, Pullman, WA 99164 USA
期刊名称：CELL REPORTS （ 影响因子：9.423； 五年影响因子：10.394 ）
ISSN： 2211-1247
年卷期： 2020 年 33 卷 9 期
页码：
收录情况： SCI
摘要： Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is correlated with higher mitochondrial content and oxidative muscle fibers in offspring muscle and improved endurance capacity. Apelin, an exerkine, is elevated due to ME, and maternal apelin administration mirrors the effect of ME on mitochondrial biogenesis in fetal muscle. Importantly, both ME and apelin induce DNA demethylation of the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (Ppargc1a) promoter and enhance its expression and mitochondrial biogenesis in fetal muscle. Such changes in DNA methylation were maintained in offspring, with ME offspring muscle expressing higher levels of PGC-1a1/4 isoforms, explaining improved muscle function. In summary, ME enhances DNA demethylation of the Ppargc1a promoter in fetal muscle, which has positive programming effects on the exercise endurance capacity and protects offspring muscle against metabolic dysfunction.
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