葡萄糖胺通过不同的信号途径抑制肌母细胞的增殖和分化，并刺激肌管萎缩。

IF 4.8 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry Pub Date : 2024-09-07 DOI:10.1016/j.jnutbio.2024.109762

Shui-Yu Liu , Luen-Kui Chen , Yi-Ting Chung , Chien-Wei Chen , Guan-Lin Wu , Yi-Chieh Chang , Pin-Rong Chen , Yuan-I Chang , Heng-Fu Lin , Liang-Yi Wu , Chi-Chang Juan

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引用次数: 0

摘要

葡萄糖胺（GlcN）是用于治疗骨关节炎的膳食补充剂之一。葡萄糖胺是由葡萄糖通过己糖胺途径合成的内源性物质。除改善关节炎外，GlcN 还具有多种生物功能，包括骨骼肌中的胰岛素抵抗。然而，GlcN 在骨骼肌发育过程中的调控作用尚不明确。因此，我们在 C2C12 细胞中研究了 GlcN 对肌母细胞增殖、分化和肌管发育的影响及其内在机制。肌细胞增殖通过 MTT 试验测定。MyoD、肌生成素（MyoG）和肌球蛋白重链（MyHC）的表达被确定为肌细胞分化的决定因素。atrogin-1和肌肉环指蛋白-1（MuRF-1）的表达被确定为肌管萎缩的标志物。结果表明，用 GlcN 处理可显著减少成肌细胞的增殖以及 Stat3 和 S6K 的磷酸化。这些发现表明，GlcN 可通过抑制 Stat3 和 S6K 的磷酸化来抑制肌母细胞的生长。此外，GlcN还能明显抑制MyoD、MyoG和MyHC的表达以及肌管的形成。用ER应激抑制剂预处理C2C12成肌细胞可明显阻止GlcN抑制的MyHC表达和肌管形成。由此可以得出结论，GlcN是通过涉及ER应激的途径抑制成肌细胞分化的。此外，GlcN还降低了C2C12肌细胞中肌管的直径和MyHC的表达，并增加了MuRF-1的表达。同时，GlcN还降低了磷酸化Akt的表达，并且在GlcN处理C2C12肌管后，mTOR受到刺激。因此，GlcN通过抑制蛋白质合成途径诱导骨骼肌萎缩。长期输注 GlcN 也会导致小鼠骨骼肌萎缩。总之，GlcN通过不同的信号通路调控骨骼肌发育的重要阶段。

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Glucosamine inhibits myoblast proliferation and differentiation, and stimulates myotube atrophy through distinct signal pathways

Glucosamine (GlcN) is one of the dietary supplements used in the treatment of osteoarthritis. Endogenously, GlcN is synthesized from glucose through the hexosamine pathway. In addition to ameliorating arthritis, several biological functions of GlcN have been reported, including insulin resistance in skeletal muscle. However, the regulatory role of GlcN in skeletal muscle development is not clear. We therefore investigated the effect of GlcN on myoblast proliferation, differentiation, and myotube development and their underlying mechanisms in C2C12 cells. Myoblast proliferation was measured by MTT assay. The expressions of MyoD, myogenin (MyoG), and myosin heavy chain (MyHC) were identified as determinants of myoblast differentiation. Expressions of atrogin-1 and muscle RING-finger protein-1 (MuRF-1) were identified as markers of myotube atrophy. The results show that treatment with GlcN significantly reduced myoblast proliferation and phosphorylation of Stat3 and S6K. These findings suggest that GlcN can inhibit growth of myoblasts through inhibiting phosphorylation of Stat3 and S6K. In addition, GlcN significantly suppressed the expression of MyoD, MyoG, and MyHC, as well as myotube formation. Pretreatment of C2C12 myoblast cells with ER stress inhibitors significantly blocked GlcN-inhibited MyHC expression and myotube formation. It can be concluded that GlcN suppressed myogenic differentiation via a pathway that involved ER stress. Moreover, GlcN decreased myotube diameter and expression of MyHC, as well as increased MuRF-1 in C2C12 myotubes. Meanwhile, GlcN also reduced the expressions of phosphorylated Akt and mTOR were stimulated after GlcN treatment in C2C12 myotubes. Thus, GlcN induced skeletal muscle atrophy by inhibiting the protein synthesis pathway. Chronic GlcN infusion also caused skeletal muscle atrophy in mice. In conclusion, GlcN regulated important stages of skeletal muscle development through different signaling pathways.

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来源期刊

Journal of Nutritional Biochemistry 医学-生化与分子生物学

CiteScore

9.50

自引率

3.60%

发文量

237

审稿时长

68 days

期刊介绍： Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.