Won Hee Choi1, Hyo Jeong Son1, Young Jin Jang1, Jiyun Ahn1,2, Chang Hwa Jung1,2, Tae Youl Ha1,2. 1. Nutrition and Metabolism Research Division, Korea Food Research Institute, Wansan-gu, Republic of Korea. 2. Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea.
Abstract
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.
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 obesemice. CONCLUSION: The results suggested that AP ameliorated the obesity-induced skeletal muscle atrophy by attenuating mitochondrial dysfunction.