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细胞因子样激素瘦素在衰老过程中肌肉与骨骼相互作用中的作用

Role of the Cytokine-like Hormone Leptin in Muscle-bone Crosstalk with Aging.

作者信息

Hamrick Mark W

机构信息

Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA, USA.

出版信息

J Bone Metab. 2017 Feb;24(1):1-8. doi: 10.11005/jbm.2017.24.1.1. Epub 2017 Feb 28.

DOI:10.11005/jbm.2017.24.1.1
PMID:28326295
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5357607/
Abstract

The cytokine-like hormone leptin is a classic adipokine that is secreted by adipocytes, increases with weight gain, and decreases with weight loss. Additional studies have, however, shown that leptin is also produced by skeletal muscle, and leptin receptors are abundant in both skeletal muscle and bone-derived mesenchymal (stromal) stem cells. These findings suggest that leptin may play an important role in muscle-bone crosstalk. Leptin treatment increases the expression of myogenic genes in primary myoblasts, and leptin treatment increases the expression of microRNAs involved in myogenesis. Bone marrow adipogenesis is associated with low bone mass in humans and rodents, and leptin can reduce marrow adipogenesis centrally through its receptors in the hypothalamus as well as directly via its receptors in bone marrow stem cells. Yet, central leptin resistance can increase with age, and low circulating levels of leptin have been observed among the frail elderly. Thus, aging appears to significantly alter leptin-mediated crosstalk among various organs and tissues. Aging is associated with bone loss and muscle atrophy, contributing to frailty, postural instability, and the incidence of falls. Therapeutic interventions such as protein and amino acid supplementation that can increase muscle mass and muscle-derived leptin may have multiple benefits for the elderly that can potentially reduce the incidence of falls and fractures.

摘要

细胞因子样激素瘦素是一种典型的脂肪因子,由脂肪细胞分泌,随体重增加而升高,随体重减轻而降低。然而,更多研究表明,骨骼肌也能产生瘦素,且瘦素受体在骨骼肌和骨源性间充质(基质)干细胞中均大量存在。这些发现提示,瘦素可能在肌肉与骨骼的相互作用中发挥重要作用。瘦素处理可增加原代成肌细胞中肌源性基因的表达,且瘦素处理可增加参与肌生成的微小RNA的表达。骨髓脂肪生成与人类和啮齿动物的低骨量相关,瘦素可通过下丘脑的受体在中枢降低骨髓脂肪生成,也可通过骨髓干细胞中的受体直接发挥作用。然而,中枢性瘦素抵抗会随年龄增长而增加,且在体弱的老年人中观察到循环瘦素水平较低。因此,衰老似乎会显著改变瘦素介导的各器官和组织间的相互作用。衰老与骨质流失和肌肉萎缩相关,会导致身体虚弱、姿势不稳和跌倒发生率增加。补充蛋白质和氨基酸等治疗性干预措施可增加肌肉量和肌肉源性瘦素,可能对老年人有多种益处, potentially reduce the incidence of falls and fractures.(原文此处表述有误,按正确逻辑翻译为)从而有可能降低跌倒和骨折的发生率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/a9a1eb47710a/jbm-24-1-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/d5a9ec3f4cc7/jbm-24-1-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/61833c9a4c46/jbm-24-1-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/a9a1eb47710a/jbm-24-1-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/d5a9ec3f4cc7/jbm-24-1-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/61833c9a4c46/jbm-24-1-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d72/5357607/a9a1eb47710a/jbm-24-1-g003.jpg

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