Apigenin Ameliorates the Obesity-Induced Skeletal Muscle Atrophy by Attenuating Mitochondrial Dysfunction in the Muscle of Obese Mice.
Mol Nutr Food Res. 2017 Oct 2. Epub 2017 Oct 2. PMID: 28971573
Won Hee Choi
SCOPE: We investigated whether apigenin protected against skeletal muscle atrophy induced by obesity.
METHODS AND RESULTS: Mice were fed a high fat diet (HFD) for 9 wks 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% apigenin-containing HFD. After additional feeding of the experimental diet for 8 wks, mice in the HFD group were highly obese compared with the mice in the standard diet fed mice group. The mice in the apigenin-treated group showed less fat pad accumulation and less inflammatory cytokines without body weight reduction. The weight of skeletal muscle in the apigenin group tended to increase compared with that of the HFD group. Furthermore, apigenin 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 apigenin. In cultured C2C12 cells, apigenin also suppressed palmitic acid-induced muscle atrophy and mitochondrial dysfunction. In addition, apigenin activated AMP-activated protein kinase (AMPK) in the C2C12 and the muscle of HFD-induced obese mice.
CONCLUSION: The results suggested that apigenin ameliorated the obesity-induced skeletal muscle atrophy by attenuating mitochondrial dysfunction. This article is protected by copyright. All rights reserved.