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Puerarin ameliorates skeletal muscle atrophy in STZ-induced type 1 diabetic rats by enhancing Akt/mTOR while inhibiting autophagy signaling pathway
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  • Lin Yin,
  • Xi Chen,
  • Na Li,
  • Weihua Jia,
  • Nuoqi Wang,
  • Biyu Hou,
  • Li Zhang,
  • Guifen Qiang,
  • Xiuying Yang,
  • Guan Hua Du
Lin Yin
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Xi Chen
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Na Li
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Weihua Jia
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Nuoqi Wang
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Biyu Hou
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Li Zhang
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Guifen Qiang
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Xiuying Yang
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Guan Hua Du
Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Materia Medica
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Abstract

Background and Purpose: Puerarin is an important isoflavone component extracted from Pueraria lobate in traditional Chinese medicine. It has a wide range of pharmacological effects. Increasing evidence indicates that puerarin alleviates hyperglycemia and numerous related complications. In this study, we explored the effect of puerarin on skeletal muscle atrophy caused by type 1 diabetes in rats. Experimental Approach: Male Sprague Dawley (SD) rats with streptozotocin (STZ)-induced type 1 diabetes were used in this study. We measured skeletal muscle weight, size and strength together with the transformation of skeletal muscle types in type 1 diabetic rats. Skeletal muscle L6 cells were used for in vitro study. Key Results: Puerarin increased muscle tissue weights and improved muscle strength. An enhanced skeletal muscle cross-sectional area was accompanied by reduced mRNA expression of muscle atrophy marker genes, including F-box only protein 32 (Atrogin-1) and muscle-specific RING-finger 1(Murf-1), both in vitro and in vivo. The transformation from type I fibers (slow muscle) to type II fibers (fast muscle) was also observed after puerarin administration. In vitro studies suggested that puerarin upregulated Akt/mTOR but downregulated the LC3/p62 signaling pathway, eventually resulting in muscle hypertrophy. Conclusions and Implications: Our study observed that puerarin mitigated skeletal muscle atrophy in type 1 diabetic rats. Subsequently, we found that the related mechanisms closely involved the upregulation of protein synthesis via the Akt/mTOR signaling pathway. Whether this anti-diabetic muscle atrophy effect in mice applies to humans remains unknown.