Critical Windows for the Programming Effects of Early-Life Nutrition on Skeletal Muscle Mass.
Critical Windows for the Programming Effects of Early-Life Nutrition on Skeletal Muscle Mass.
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DOI：
10.1159/000486490
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发表时间：
2018-01-01
影响因子：
--
通讯作者：
Davis, Teresa A
中科院分区：
文献类型：
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作者：
Fiorotto, Marta L;Davis, Teresa A
骨骼肌发生始于胚胎，伴随着肌肉祖细胞的增殖和分化，最终融合形成多核肌纤维。妊娠中期后，肌肉生长通过这些肌纤维的肥大发生。最快速的生长阶段发生在围产期，导致肌肉质量从出生时的瘦体重的25%扩展到成熟时的40-45%。肌肉生长的这两个阶段由细胞外信号和细胞内信号通路及其激活的调控网络参与的不同分子机制调节。营养素通过提供必要的底物和引发细胞外信号来影响肌肉生长，细胞外信号调节控制纤维合成代谢过程的信号转导途径。未成熟肌纤维肥大的独特的大容量是由蛋白质合成对喂养诱导的血浆胰岛素和氨基酸变化的提高的能力和敏感性以及通过肌肉前体细胞（卫星细胞）增殖来扩大其肌纤维群的能力实现的。随着成熟，卫星细胞变得静止，限制了肌肉的生长，肌肉蛋白质合成的能力逐渐减弱。因此，早期发育阶段代表肌肉生长的关键窗口，如果中断，则导致不太可能完全恢复的肌肉质量缺陷。
Skeletal myogenesis begins in the embryo with proliferation and differentiation of muscle progenitor cells that ultimately fuse to form multinucleated myofibers. After midgestation, muscle growth occurs through hypertrophy of these myofibers. The most rapid growth phase occurs in the perinatal period, resulting in the expansion of muscle mass from 25% of lean mass at birth to 40-45% at maturity. These 2 phases of muscle growth are regulated by distinct molecular mechanisms engaged by extracellular cues and intracellular signaling pathways and regulatory networks they activate. Nutrients influence muscle growth by both providing the necessary substrates and eliciting extracellular cues which regulate the signal transduction pathways that control the anabolic processes of the fibers. The uniquely large capacity of immature myofibers for hypertrophy is enabled by a heightened capacity and sensitivity of protein synthesis to feeding-induced changes in plasma insulin and amino acids, and the ability to expand their myonuclear population through proliferation of muscle precursor cells (satellite cells). With maturation, satellite cells become quiescent, limiting myonuclear accretion, and the capacity of the muscles for protein anabolism progressively diminishes. Therefore, the early developmental phases represent critical windows for muscle growth which, if disrupted, result in muscle mass deficits that are unlikely to be entirely recoverable.