Nutrition and Metabolism Research Division, Korea Food Research Institute, Wansan-gu, Republic of Korea.
Division of Food Biotechnology, University of Science and Technology, Daejeon, Republic of Korea.
Mol Nutr Food Res. 2017 Dec;61(12). doi: 10.1002/mnfr.201700218. Epub 2017 Nov 2.
It was investigated whether apigenin (AP) protected against skeletal muscle atrophy induced by obesity.
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.
The results suggested that AP ameliorated the obesity-induced skeletal muscle atrophy by attenuating mitochondrial dysfunction.
研究了芹菜素 (AP) 是否能预防肥胖引起的骨骼肌萎缩。
将小鼠用高脂肪饮食 (HFD) 喂养 9 周以诱导肥胖，然后将其分为两组；HFD 组给予高脂肪饮食，HFD+AP 组给予含 0.1% AP 的高脂肪饮食。在额外喂食实验饮食 8 周后，与标准饮食喂养的小鼠相比，HFD 组的小鼠高度肥胖。与 HFD 组相比，AP 处理组的脂肪垫积累较少，炎症细胞因子较少，体重无减轻。AP 组骨骼肌重量呈增加趋势。此外，AP 降低了萎缩基因的表达，包括 MuRF1 和 Atrogin-1，但增加了运动能力。AP 增强了线粒体功能和线粒体生物发生。在培养的 C2C12 细胞中，AP 还抑制了棕榈酸诱导的肌肉萎缩和线粒体功能障碍。此外，AP 激活了 C2C12 和 HFD 诱导肥胖小鼠肌肉中的 AMP 激活的蛋白激酶 (AMPK)。
结果表明，AP 通过减轻线粒体功能障碍改善了肥胖引起的骨骼肌萎缩。
