ABSTRACT Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) modulate cellular metabolic functions and gene expression. This study investigated the impacts of EPA and DHA on gene expression and morphological changes during adipogenic inducement in C2C12 myoblasts. Cells were cultured and treated with differentiation medium with and without 50 μM EPA and DHA. Cells treated with fatty acids had noticeable lipid droplets, but no formation of myotubes compared to control group cells. The expression levels of key genes relevant to adipogenesis and inflammation were significantly higher (P < 0.05) in cells treated with fatty acids. Genes associated with myogenesis and mitochondrial biosynthesis and function had lower (P < 0.05) expression with fatty acids supplementation. Moreover, fatty acid treatment reduced (P < 0.05) oxygen consumption rate in the differentiated cells. This suggested blocking myotube formation through supplementation with EPA and DHA drove myoblasts to enter the quiescent state and enabled adipogenic trans-differentiation of the myoblasts. Data also suggested that overdosage of EPA and DHA during gestation may drive fetal mesenchymal stem cell differentiation to the fate of adipogenesis and have a long-term effect on childhood obesity.

中文翻译：

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二十碳五烯酸和二十二碳六烯酸对C2C12细胞脂肪生成和肌管形成抑制的影响

摘要 二十碳五烯酸 (EPA) 和二十二碳六烯酸 (DHA) 调节细胞代谢功能和基因表达。本研究调查了 EPA 和 DHA 对 C2C12 成肌细胞成脂诱导过程中基因表达和形态变化的影响。培养细胞并用含有和不含 50 μM EPA 和 DHA 的分化培养基处理。用脂肪酸处理的细胞具有明显的脂滴，但与对照组细胞相比没有形成肌管。在用脂肪酸处理的细胞中，与脂肪生成和炎症相关的关键基因的表达水平显着升高（P < 0.05）。与肌生成和线粒体生物合成和功能相关的基因在补充脂肪酸的情况下表达较低（P < 0.05）。此外，脂肪酸处理减少（P < 0. 05) 分化细胞的耗氧率。这表明通过补充 EPA 和 DHA 来阻止肌管形成，驱使成肌细胞进入静止状态，并使成肌细胞的成脂转分化成为可能。数据还表明，妊娠期间过量服用 EPA 和 DHA 可能会促使胎儿间充质干细胞分化为脂肪生成的命运，并对儿童肥胖产生长期影响。