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An obesogenic maternal environment impairs mouse growth patterns, satellite cell activation and markers of post-natal myogenesis.
American Journal of Physiology-Endocrinology and Metabolism ( IF 4.2 ) Pub Date : 2020-09-21 , DOI: 10.1152/ajpendo.00398.2020
Jasmine Mikovic 1 , Camille Brightwell 2 , Angus Lindsay 1 , Yuan Wen 2 , Greg Kowalski 1 , Aaron P Russell 1 , Christopher S Fry 2 , Séverine Lamon 1
Affiliation  

Skeletal muscle is sensitive to environmental cues that are first present in utero. Maternal over-nutrition is a model of impaired muscle development leading to structural and metabolic dysfunction in adult life. In this study, we investigated the effect of an obesogenic maternal environment on growth and post-natal myogenesis in the offspring. Male C57BL/6J mice born to chow or high-fat fed mothers were allocated to four different groups at the end of weaning. For the following ten weeks, half of the pups were maintained on the same diet as their mother and half of the pups were switched to the other diet (chow or high-fat). At 12 weeks of age, muscle injury was induced using an intramuscular injection of barium chloride. Seven days later, mice were humanely killed and muscle tissue was harvested. A high-fat maternal diet impaired offspring growth patterns and downregulated satellite cell activation and markers of post-natal myogenesis seven days after injury without altering the number of newly synthetized fibres over the whole seven-day period. Importantly, a healthy post-natal diet could not reverse any of these effects. In addition, we demonstrated that post-natal myogenesis was associated with a diet-independent upregulation of three miRNAs, mmu-miR-31-5p, mmu-miR-136-5p and mmu-miR-296-5p. Further in vitro analysis confirmed the role of these miRNAs in myocyte proliferation. Our findings are the first to demonstrate that maternal over-nutrition impairs markers of post-natal myogenesis in the offspring, and are particularly relevant to today's society where the incidence of overweight/obesity in women of child-bearing age is increasing.

中文翻译:

致孕的产妇环境会损害小鼠的生长方式,卫星细胞的活化以及出生后肌生成的标记。

骨骼肌对子宫中首先存在的环境提示敏感。孕产妇过度营养是导致成人发育中结构和代谢功能障碍的肌肉发育受损的模型。在这项研究中,我们调查了肥胖的母体环境对后代生长和产后肌生成的影响。由断奶或高脂喂养的母亲出生的雄性C57BL / 6J小鼠在断奶结束时被分为四个不同的组。在接下来的十周中,一半的幼仔与母亲保持相同的饮食,一半的幼仔改为其他饮食(低脂或高脂)。在12周龄时,肌肉注射氯化钡会引起肌肉损伤。七天后,将人道杀害小鼠并收获肌肉组织。高脂孕妇饮食在损伤后7天损害了后代的生长方式,降低了卫星细胞的活化和出生后肌生成的标志,而在整个7天内未改变新合成纤维的数量。重要的是,健康的产后饮食不能逆转这些影响。此外,我们证明了产后肌发生与三种miRNA,mmu-miR-31-5p,mmu-miR-136-5p和mmu-miR-296-5p的饮食独立上调有关。进一步的体外分析证实了这些miRNA在肌细胞增殖中的作用。我们的发现是第一个证明母亲过度营养会损害后代产后肌生成的标志物的研究结果,并且与今天的研究特别相关。
更新日期:2020-09-22
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