Division of Biofunctional Sciences, Department of Integrated Health Sciences, Graduate School of Medicine, Nagoya University, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, Aichi 461-0047, Japan.
Division of Morphological Sciences, Kagoshima University Graduate School of Medicine and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan.
Int J Mol Sci. 2021 Mar 18;22(6):3110. doi: 10.3390/ijms22063110.
Cachexia is a multifactorial syndrome characterized by muscle loss that cannot be reversed by conventional nutritional support. To uncover the molecular basis underlying the onset of cancer cachectic muscle wasting and establish an effective intervention against muscle loss, we used a cancer cachectic mouse model and examined the effects of aerobic exercise. Aerobic exercise successfully suppressed muscle atrophy and activated adiponectin signaling. Next, a cellular model for cancer cachectic muscle atrophy using C2C12 myotubes was prepared by treating myotubes with a conditioned medium from a culture of colon-26 cancer cells. Treatment of the atrophic myotubes with recombinant adiponectin was protective against the thinning of cells through the increased production of p-mTOR and suppression of LC3-II. Altogether, these findings suggest that the activation of adiponectin signaling could be part of the molecular mechanisms by which aerobic exercise ameliorates cancer cachexia-induced muscle wasting.
恶病质是一种多因素综合征，其特征是肌肉减少，常规营养支持无法逆转。为了揭示癌症恶病质肌肉减少的发病机制基础，并建立针对肌肉减少的有效干预措施，我们使用了癌症恶病质小鼠模型，并研究了有氧运动的效果。有氧运动成功抑制了肌肉萎缩并激活了脂联素信号。接下来，通过用结肠-26 癌细胞培养的条件培养基处理肌管，制备了用于癌症恶病质肌肉萎缩的细胞模型。重组脂联素处理萎缩的肌管可通过增加 p-mTOR 的产生和抑制 LC3-II 来防止细胞变薄。总的来说，这些发现表明，脂联素信号的激活可能是有氧运动改善癌症恶病质引起的肌肉减少的分子机制的一部分。
