Jung Su-Ryun
Senotherapy-based Metabolic Disease Control Research Center, College of Medicine, Yeungnam University, Daegu, Republic of Korea.
Phys Act Nutr. 2025 Jun;29(2):19-25. doi: 10.20463/pan.2025.0010. Epub 2025 Jun 30.
We provided basic scientific data to help prevent and treat sarcopenia in young obese individuals by observing the effects of low-intensity endurance exercise and low-dose lithium treatment on skeletal muscle atrophy in rats with high-fat diet (HFD)-induced obesity.
Six-week-old male Wistar rats were fed an HFD for 8 weeks to induce obesity. Next, rats were randomly assigned to four groups and treated with lithium or exercise for 8 weeks. Lithium (10 mg/kg lithium chloride [LiCl], gavage) or endurance exercise (17 m/min, 30 min/day) was performed once daily for 5 days per week. After the experiment, body composition was measured using dual-energy X-ray absorptiometry (DEXA), and tissues were extracted after anesthesia and analyzed.
Endurance exercise or 8 weeks of lithium had no significant effect on the morphology of the liver and kidney tissues in rats. Although lithium and endurance exercises alone increased the lean body mass, the difference was not statistically significant. However, combined treatment with lithium and endurance exercise significantly increased the lean body mass. No significant difference was noted in the abdominal fat mass between the groups. Eight weeks of lithium or endurance exercise did not affect the mechanistic target of rapamycin (mTOR) expression in the skeletal muscles of obese rats. However, it significantly inhibited the FOXO1 signaling pathway, a muscle atrophy signal, and reduced the expression of tumor necrosis factor (TNF) α.
A combination of low-intensity endurance exercise and low-dose lithium prevented muscle atrophy (wasting) by inhibiting the FOXO1 signaling pathway in skeletal muscles. Therefore, light walking and lithium supplementation in daily life are expected to prevent muscle atrophy in obese patients. However, it is difficult to draw definitive conclusions based on the results of this study alone and additional research is warranted.
通过观察低强度耐力运动和低剂量锂治疗对高脂饮食（HFD）诱导肥胖大鼠骨骼肌萎缩的影响，提供基础科学数据，以帮助预防和治疗年轻肥胖个体的肌肉减少症。
六周龄雄性Wistar大鼠喂食HFD 8周以诱导肥胖。接下来，将大鼠随机分为四组，并用锂或运动治疗8周。锂（10mg/kg氯化锂[LiCl]，灌胃）或耐力运动（17m/min，每天30分钟）每周进行5天，每天一次。实验结束后，使用双能X射线吸收法（DEXA）测量身体成分，并在麻醉后提取组织并进行分析。
耐力运动或8周锂治疗对大鼠肝脏和肾脏组织的形态没有显著影响。虽然单独使用锂和耐力运动增加了瘦体重，但差异没有统计学意义。然而，锂和耐力运动联合治疗显著增加了瘦体重。各组之间腹部脂肪量没有显著差异。8周的锂或耐力运动对肥胖大鼠骨骼肌中雷帕霉素的机械靶点（mTOR）表达没有影响。然而，它显著抑制了FOXO1信号通路，这是一种肌肉萎缩信号，并降低了肿瘤坏死因子（TNF）α的表达。
低强度耐力运动和低剂量锂的联合通过抑制骨骼肌中的FOXO1信号通路预防了肌肉萎缩（消瘦）。因此，日常生活中的轻度步行和补充锂有望预防肥胖患者的肌肉萎缩。然而，仅根据本研究结果很难得出明确结论，需要进一步的研究。
