Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, UK.
Nutrients. 2021 Feb 25;13(3):729. doi: 10.3390/nu13030729.
Childhood growth and its sensitivity to dietary protein is reviewed within a Protein-Stat model of growth regulation. The coordination of growth of muscle and stature is a combination of genetic programming, and of two-way mechanical interactions involving the mechanotransduction of muscle growth through stretching by bone length growth, the core Protein-Stat feature, and the strengthening of bone through muscle contraction via the mechanostat. Thus, growth in bone length is the initiating event and this is always observed. Endocrine and cellular mechanisms of growth in stature are reviewed in terms of the growth hormone-insulin like growth factor-1 (GH-IGF-1) and thyroid axes and the sex hormones, which together mediate endochondral ossification in the growth plate and bone lengthening. Cellular mechanisms of muscle growth during development are then reviewed identifying (a) the difficulties posed by the need to maintain its ultrastructure during myofibre hypertrophy within the extracellular matrix and the concept of muscle as concentric "bags" allowing growth to be conceived as bag enlargement and filling, (b) the cellular and molecular mechanisms involved in the mechanotransduction of satellite and mesenchymal stromal cells, to enable both connective tissue remodelling and provision of new myonuclei to aid myofibre hypertrophy and (c) the implications of myofibre hypertrophy for protein turnover within the myonuclear domain. Experimental data from rodent and avian animal models illustrate likely changes in DNA domain size and protein turnover during developmental and stretch-induced muscle growth and between different muscle fibre types. Growth of muscle in male rats during adulthood suggests that "bag enlargement" is achieved mainly through the action of mesenchymal stromal cells. Current understanding of the nutritional regulation of protein deposition in muscle, deriving from experimental studies in animals and human adults, is reviewed, identifying regulation by amino acids, insulin and myofibre volume changes acting to increase both ribosomal capacity and efficiency of muscle protein synthesis via the mechanistic target of rapamycin complex 1 (mTORC1) and the phenomenon of a "bag-full" inhibitory signal has been identified in human skeletal muscle. The final section deals with the nutritional sensitivity of growth of muscle and stature to dietary protein in children. Growth in length/height as a function of dietary protein intake is described in the context of the breastfed child as the normative growth model, and the "Early Protein Hypothesis" linking high protein intakes in infancy to later adiposity. The extensive paediatric studies on serum IGF-1 and child growth are reviewed but their clinical relevance is of limited value for understanding growth regulation; a role in energy metabolism and homeostasis, acting with insulin to mediate adiposity, is probably more important. Information on the influence of dietary protein on muscle mass per se as opposed to lean body mass is limited but suggests that increased protein intake in children is unable to promote muscle growth in excess of that linked to genotypic growth in length/height. One possible exception is milk protein intake, which cohort and cross-cultural studies suggest can increase height and associated muscle growth, although such effects have yet to be demonstrated by randomised controlled trials.
儿童生长及其对膳食蛋白质的敏感性是在生长调控的蛋白质稳态模型中进行综述的。肌肉和身高的生长协调是遗传编程的组合,以及涉及通过骨生长拉伸来实现肌肉生长的机械转导、核心蛋白质稳态特征,以及通过肌肉收缩通过机械稳定器增强骨骼的双向机械相互作用的组合。因此,骨长度的生长是起始事件,这是始终观察到的。从生长激素-胰岛素样生长因子-1(GH-IGF-1)和甲状腺轴以及性激素的角度,综述了身高生长的内分泌和细胞机制,这些机制共同介导生长板和骨延长过程中的软骨内骨化。然后,回顾了发育过程中肌肉生长的细胞机制,确定了 (a) 在细胞外基质中维持肌纤维肥大期间超微结构的需要所带来的困难,以及将肌肉视为同心“袋”的概念,允许将生长视为袋膨胀和填充,(b) 卫星细胞和间充质基质细胞的机械转导所涉及的细胞和分子机制,以实现结缔组织重塑和提供新的肌核,以辅助肌纤维肥大,以及 (c) 肌纤维肥大对肌核域内蛋白质周转的影响。来自啮齿动物和禽类动物模型的实验数据说明了在发育和拉伸诱导的肌肉生长过程中以及不同肌肉纤维类型之间,DNA 结构域大小和蛋白质周转的可能变化。成年雄性大鼠的肌肉生长表明,“袋膨胀”主要通过间充质基质细胞的作用来实现。从动物和成年人类的实验研究中,综述了对肌肉中蛋白质沉积的营养调节的理解,确定了氨基酸、胰岛素和肌纤维体积变化的调节作用,通过机械靶标雷帕霉素复合物 1(mTORC1) 增加核糖体的容量和肌肉蛋白质合成的效率,并且在人类骨骼肌中已经确定了“袋满”抑制信号的现象。最后一部分涉及儿童肌肉和身高生长对膳食蛋白质的营养敏感性。以母乳喂养儿童为规范生长模型,描述了作为膳食蛋白质摄入量的功能的长度/身高生长,以及将婴儿期高蛋白摄入与后期肥胖联系起来的“早期蛋白质假说”。综述了关于血清 IGF-1 和儿童生长的广泛儿科研究,但它们的临床相关性对于理解生长调节的价值有限;在能量代谢和稳态中发挥作用,与胰岛素一起介导肥胖,可能更为重要。关于膳食蛋白质对肌肉质量本身而不是瘦体重的影响的信息有限,但表明儿童摄入更多的蛋白质并不能促进超出与长度/身高相关的基因型生长的肌肉生长。一个可能的例外是牛奶蛋白摄入,队列和跨文化研究表明,牛奶蛋白摄入可以增加身高和相关的肌肉生长,尽管这种影响尚未通过随机对照试验证明。