Duchenne muscular dystrophy (DMD) is an intractable genetic disease associated with progressive skeletal muscle weakness and degeneration. Recently, it was reported that intraperitoneal injections of ketone bodies partially ameliorated muscular dystrophy by increasing satellite cell (SC) proliferation. Here, we evaluated whether a ketogenic diet (KD) with medium-chain triglycerides (MCT-KD) could alter genetically mutated DMD in model rats. We found that the MCT-KD significantly increased muscle strength and fiber diameter in these rats. The MCT-KD significantly suppressed the key features of DMD, namely, muscle necrosis, inflammation, and subsequent fibrosis. Immunocytochemical analysis revealed that the MCT-KD promoted the proliferation of muscle SCs, suggesting enhanced muscle regeneration. The muscle strength of DMD model rats fed with MCT-KD was significantly improved even at the age of 9 months. Our findings suggested that the MCT-KD ameliorates muscular dystrophy by inhibiting myonecrosis and promoting the proliferation of muscle SCs. As far as we can ascertain, this is the first study to apply a functional diet as therapy for DMD in experimental animals. Further studies are needed to elucidate the underlying mechanisms of the MCT-KD-induced improvement of DMD.

中文翻译：

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含中链甘油三酯的生酮饮食可恢复杜氏肌营养不良大鼠模型的骨骼肌功能和病理

杜氏肌营养不良症 (DMD) 是一种与进行性骨骼肌无力和退化相关的难治性遗传疾病。最近，据报道，腹膜内注射酮体可通过增加卫星细胞 (SC) 增殖来部分改善肌营养不良症。在这里，我们评估了含中链甘油三酯 (MCT-KD) 的生酮饮食 (KD) 是否可以改变模型大鼠的基因突变 DMD。我们发现 MCT-KD 显着增加了这些大鼠的肌肉力量和纤维直径。MCT-KD 显着抑制了 DMD 的关键特征，即肌肉坏死、炎症和随后的纤维化。免疫细胞化学分析显示 MCT-KD 促进了肌肉 SCs 的增殖，表明增强了肌肉再生。喂食MCT-KD的DMD模型大鼠的肌肉力量即使在9个月大时也有显着改善。我们的研究结果表明，MCT-KD 通过抑制肌坏死和促进肌肉 SCs 的增殖来改善肌营养不良症。据我们所知，这是第一项在实验动物中应用功能性饮食治疗 DMD 的研究。需要进一步的研究来阐明 MCT-KD 诱导的 DMD 改善的潜在机制。