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Apigenin Ameliorates the Obesity‐Induced Skeletal Muscle Atrophy by Attenuating Mitochondrial Dysfunction in the Muscle of Obese Mice
Author(s) -
Choi Won Hee,
Son Hyo Jeong,
Jang Young Jin,
Ahn Jiyun,
Jung Chang Hwa,
Ha Tae Youl
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700218
Subject(s) - endocrinology , medicine , skeletal muscle , mitochondrial biogenesis , muscle atrophy , ampk , amp activated protein kinase , atrophy , myocyte , mitochondrion , chemistry , biology , protein kinase a , kinase , biochemistry
Scope It was investigated whether apigenin (AP) protected against skeletal muscle atrophy induced by obesity. Methods and results Mice were fed a high‐fat diet (HFD) for 9 weeks to induce obesity, and then were assigned to two groups; the HFD group received a high‐fat diet, and the HFD+AP group received a 0.1% AP‐containing HFD. After additional feeding of the experimental diet for 8 weeks, mice in the HFD group were highly obese compared with the mice in the standard diet fed mice group. The mice in the AP‐treated group showed less fat pad accumulation and less inflammatory cytokines without body weight reduction. The weight of skeletal muscle in the AP group tended to increase as compared with that of the HFD group. Furthermore, AP reduced the expression of atrophic genes, including MuRF1 and Atrogin‐1 , but increased the exercise capacity. The mitochondrial function and mitochondrial biogenesis were enhanced by AP. In cultured C2C12 cells, AP also suppressed palmitic acid‐induced muscle atrophy and mitochondrial dysfunction. In addition, AP activated AMP‐activated protein kinase (AMPK) in the C2C12 and the muscle of HFD‐induced obese mice. Conclusion The results suggested that AP ameliorated the obesity‐induced skeletal muscle atrophy by attenuating mitochondrial dysfunction.