The combination of sarcopenia and obesity (i.e., sarcopenic obesity) is more strongly associated with disability and metabolic/cardiovascular diseases than obesity or sarcopenia alone. Therefore, countermeasures that simultaneously suppress fat gain and muscle atrophy to prevent an increase in sarcopenic obesity are warranted. The aim of this study was to investigate the simultaneous effects of fucoxanthinol (FXOH) on fat loss in mature adipocytes and the inhibition of atrophy and loss in myotubes induced by oxidative stress. C2C12 myotubes were treated with FXOH for 24 h and further incubated with hydrogen peroxide (H2O2) for 24 h. The area of myosin heavy chain-positive myotubes and the ROS concentration were measured. Mature 3T3-L1 adipocytes were treated with FXOH for 72 h. The triacylglycerol (TG) content and glycerol and fatty acid (FA) release were biochemically measured. The myotube area was smaller in H2O2-treated cells than that in control cells. However, FXOH protected against the H2O2-induced decreases in myotube area. Further, the ROS concentration was significantly higher in the FXOH-treated cells compared with that in the control cells, although it was significantly lower than that in the H2O2-treated cells. On the other hand, in the mature adipocytes, the TG content was significantly decreased by FXOH treatment compared to that in the control. Moreover, FXOH treatment significantly increased glycerol and FA release compared with that of the control. These results suggest that FXOH inhibits H2O2-induced atrophy and loss in myotubes and activates lipolysis and decreases the TG content in mature adipocytes. Accordingly, FXOH has the potential to exert anti-sarcopenic obesity effects.

中文翻译：

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岩藻黄质醇可减轻氧化应激引起的肌管萎缩和损失，并减少成熟脂肪细胞中三酰基甘油的含量。

肌肉减少症和肥胖症（即肌肉减少症）的组合比单独的肥胖症或肌肉减少症与残疾和代谢/心血管疾病的关联更强。因此，必须采取能同时抑制脂肪增加和肌肉萎缩以防止肌肉减少症肥胖症增加的对策。这项研究的目的是研究岩藻黄质醇（FXOH）对成熟脂肪细胞脂肪损失以及氧化应激诱导的肌管萎缩和损失的抑制作用。C2C12肌管用FXOH处理24小时，然后再用过氧化氢（H2O2）孵育24小时。测量肌球蛋白重链阳性肌管的面积和ROS浓度。成熟的3T3-L1脂肪细胞用FXOH处理72小时。对三酰基甘油（TG）的含量以及甘油和脂肪酸（FA）的释放进行了生化测量。H2O2处理细胞的肌管面积比对照细胞小。但是，FXOH可以防止H2O2引起的肌管面积减少。此外，尽管经FXOH处理的细胞中的ROS浓度明显低于经H 2 O 2处理的细胞中的ROS浓度，但与对照细胞相比，其ROS浓度显着更高。另一方面，与对照组相比，通过FXOH处理，在成熟的脂肪细胞中TG含量显着降低。而且，与对照相比，FXOH处理显着增加了甘油和FA的释放。这些结果表明，FXOH抑制H2O2引起的肌管萎缩和丢失，并激活脂解作用并降低成熟脂肪细胞中的TG含量。