Bonjour Jean-Philippe
Horm Mol Biol Clin Investig. 2016 Oct 1;28(1):39-53. doi: 10.1515/hmbci-2016-0003.
Dietary protein represents an important nutrient for bone health and thereby for the prevention of osteoporosis. Besides its role as a brick provider for building the organic matrix of skeletal tissues, dietary protein stimulates the production of the anabolic bone trophic factor IGF-I (insulin-like growth factor I). The liver is the main source of circulating IGF-I. During growth, protein undernutrition results in reduced bone mass and strength. Genetic defect impairing the production of IGF-I markedly reduces bone development in both length and width. The serum level of IGF-I markedly increases and then decreases during pubertal maturation in parallel with the change in bone growth and standing height velocity. The impact of physical activity on bone structure and strength is enhanced by increased dietary protein consumption. This synergism between these two important environmental factors can be observed in prepubertal boys, thus modifying the genetically determined bone growth trajectory. In anorexia nervosa, IGF-I is low as well as bone mineral mass. In selective protein undernutrition, there is a resistance to the exogenous bone anabolic effect of IGF-I. A series of animal experiments and human clinical trials underscore the positive effect of increased dietary intake of protein on calcium-phosphate economy and bone balance. On the contrary, the dietary protein-induced acidosis hypothesis of osteoporosis is not supported by several experimental and clinical studies. There is a direct effect of amino acids on the local production of IGF-I by osteoblastic cells. IGF-I is likely the main mediator of the positive effect of parathyroid hormone (PTH) on bone formation, thus explaining the reduction in fragility fractures as observed in PTH-treated postmenopausal women. In elderly women and men, relatively high protein intake protects against spinal and femoral bone loss. In hip fracture patients, isocaloric correction of the relatively low protein intake results in: increased IGF-I serum level, significant attenuation of postsurgical bone loss, improved muscle strength, better recovery, and shortened hospital stay. Thus, dietary protein contributes to bone health from early childhood to old age. An adequate intake of protein should be recommended in the prevention and treatment of osteoporosis.
膳食蛋白质是对骨骼健康以及预防骨质疏松症而言重要的营养素。除了作为构建骨骼组织有机基质的原料提供者这一作用外，膳食蛋白质还能刺激合成代谢的骨营养因子胰岛素样生长因子I（IGF-I）的产生。肝脏是循环中IGF-I的主要来源。在生长过程中，蛋白质摄入不足会导致骨量和骨强度降低。损害IGF-I产生的基因缺陷会显著降低骨骼在长度和宽度方面的发育。在青春期成熟过程中，IGF-I的血清水平会随着骨生长和身高增长速度的变化而显著升高，然后下降。增加膳食蛋白质的摄入量可增强身体活动对骨骼结构和强度的影响。在青春期前男孩中可以观察到这两个重要环境因素之间的这种协同作用，从而改变由基因决定的骨骼生长轨迹。在神经性厌食症中，IGF-I水平较低，骨矿物质含量也低。在选择性蛋白质摄入不足的情况下，机体对外源性IGF-I的骨合成代谢作用存在抵抗。一系列动物实验和人体临床试验强调了增加膳食蛋白质摄入量对钙磷代谢和骨平衡的积极作用。相反，骨质疏松症的膳食蛋白质诱导酸中毒假说并未得到多项实验和临床研究的支持。氨基酸对成骨细胞局部产生IGF-I有直接作用。IGF-I可能是甲状旁腺激素（PTH）对骨形成产生积极作用的主要介质，这就解释了在接受PTH治疗的绝经后女性中观察到的脆性骨折减少的现象。在老年女性和男性中，相对较高的蛋白质摄入量可预防脊柱和股骨骨质流失。在髋部骨折患者中，对相对较低的蛋白质摄入量进行等热量校正会导致：IGF-I血清水平升高、术后骨质流失显著减轻、肌肉力量改善、恢复更好以及住院时间缩短。因此，从幼儿期到老年期，膳食蛋白质都有助于骨骼健康。在骨质疏松症的预防和治疗中，应建议摄入充足的蛋白质。
