A large number of studies have shown that polyphenols can regulate skeletal muscle fiber type transformation through AMPK signal. However, the effects and mechanism of naringin (a natural polyphenol) on muscle fiber type transformation still remains unclear. Thus, we hypothesized that naringin would induce the transformation of skeletal muscle fibers from type II to type I by AMPK signaling. C2C12 myotubes and BALB/c mice models were used to test this hypothesis. We found that naringin significantly increased the protein expression of slow myosin heavy chain (MyHC), myoglobin and troponin I type I slow skeletal (Troponin I-SS) and the activities of succinate dehydrogenase (SDH) and malate dehydrogenase (MDH), and significantly decreased fast MyHC protein expression and lactate dehydrogenase (LDH) activity, accompanied by the activation of AMPK and the activity of peroxisome proliferator activated receptor-γ coactivator-1α (PGC-1α) in mice and C2C12 myotubes. Further inhibition of AMPK activity by compound C showed that the above effects were significantly inhibited in C2C12 myotubes. In conclusion, naringin promotes the transformation of skeletal muscle fibers from type II to type I through AMPK/PGC-1α signaling pathway, which not only enriches the nutritional and physiological functions of naringin, but also provides a theoretical basis for the regulation of muscle fiber type transformation by nutritional approaches.

大量研究表明，多酚可以通过AMPK信号调节骨骼肌纤维类型转化。然而，柚皮苷（一种天然多酚）对肌纤维类型转变的影响和机制仍不清楚。因此，我们假设柚皮苷会通过 AMPK 信号诱导骨骼肌纤维从 II 型向 I 型的转变。使用 C2C12 肌管和 BALB/c 小鼠模型来检验这一假设。我们发现柚皮苷显着增加慢肌球蛋白重链（MyHC）、肌红蛋白和肌钙蛋白 I 型慢骨骼（肌钙蛋白 I-SS）的蛋白表达以及琥珀酸脱氢酶（SDH）和苹果酸脱氢酶（MDH）的活性，并显着增加在小鼠和 C2C12 肌管中，快速 MyHC 蛋白表达和乳酸脱氢酶 (LDH) 活性降低，同时伴有 AMPK 激活和过氧化物酶体增殖物激活受体-γ 共激活剂-1α (PGC-1α) 活性。化合物C进一步抑制AMPK活性表明，在C2C12肌管中上述作用受到显着抑制。综上所述，柚皮苷通过AMPK/PGC-1α信号通路促进骨骼肌纤维由II型向I型转变，不仅丰富了柚皮苷的营养和生理功能，而且为肌纤维的调控提供了理论依据。通过营养方法进行类型转变。