Kim Changhee, Kim Mi-Bo, Lee Sanggil, Hwang Jae-Kwan
Department of Biotechnology, Yonsei University, Seoul 03722, Republic of Korea.
Graduate Program in Bioindustrial Engineering, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea.
Nutrients. 2025 Aug 14;17(16):2642. doi: 10.3390/nu17162642.
: Sarcopenic obesity, defined by the coexistence of excessive fat accumulation and progressive muscle loss, is associated with an increased risk of metabolic dysfunction and physical disability. While 5,7-dimethoxyflavone (DMF), a bioactive flavone derived from , has demonstrated anti-obesity and muscle-preserving properties, its effects on sarcopenic obesity remain unclear. : Four-week-old male C57BL/6J mice were fed a high-fat diet (HFD) for 6 weeks to induce sarcopenic obesity, followed by 8 weeks of continued HFD with the oral administration of DMF. Muscle function was assessed through grip strength and treadmill running tests, while muscle and fat volumes were measured using micro-CT. Mechanistic analyses were performed using gene expression and Western blot analysis. : DMF significantly reduced body weight, fat mass, and adipocyte size while enhancing grip strength, endurance, skeletal muscle mass, and the muscle fiber cross-sectional area. In the gastrocnemius muscle, DMF increased the gene expression of () and its isoform , thereby promoting mitochondrial biogenesis. It also improved protein turnover by modulating protein synthesis and degradation via the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. In subcutaneous and brown adipose tissues, DMF increased mitochondrial DNA content and the expression of thermogenic and beige adipocyte-related genes. These findings suggest that DMF alleviates sarcopenic obesity by improving mitochondrial function and regulating energy metabolism in both skeletal muscle and adipose tissues via PGC-1α-mediated pathways. Thus, DMF represents a promising therapeutic candidate for the integrated management of sarcopenic obesity.
肌少症性肥胖定义为脂肪过度堆积与进行性肌肉流失并存，与代谢功能障碍和身体残疾风险增加相关。虽然5,7 - 二甲氧基黄酮（DMF）是一种从[来源未提及]衍生的生物活性黄酮，已显示出抗肥胖和保留肌肉的特性，但其对肌少症性肥胖的影响仍不清楚。
四周龄雄性C57BL / 6J小鼠喂食高脂饮食（HFD）6周以诱导肌少症性肥胖，随后继续HFD 8周并口服DMF。通过握力和跑步机跑步测试评估肌肉功能，同时使用微型计算机断层扫描（micro - CT）测量肌肉和脂肪体积。使用基因表达和蛋白质印迹分析进行机制分析。
DMF显著降低体重、脂肪量和脂肪细胞大小，同时增强握力、耐力、骨骼肌质量和肌纤维横截面积。在腓肠肌中，DMF增加了[基因名称未提及]及其同工型的基因表达，从而促进线粒体生物发生。它还通过磷脂酰肌醇3 - 激酶/蛋白激酶B/雷帕霉素机制靶点信号通路调节蛋白质合成和降解，改善蛋白质周转。在皮下和棕色脂肪组织中，DMF增加线粒体DNA含量以及产热和米色脂肪细胞相关基因的表达。这些发现表明，DMF通过改善线粒体功能并通过PGC - 1α介导的途径调节骨骼肌和脂肪组织中的能量代谢来减轻肌少症性肥胖。因此，DMF是肌少症性肥胖综合管理的一个有前景的治疗候选物。
