Obesity causes the development of insulin resistance and type 2 diabetes. Phosphatidylcholine (PPC) has been reported to increase hepatic insulin sensitivity and lipolysis in adipose tissue to resolve local obesity. In this study, we proposed 1,2-dilinoleoyl-sn-glycero-3-phosphocholine (DLPC), the main active species of PPC, as an effective substance for the treatment of obesity-mediated disorders such as impaired fat metabolism and insulin resistance. Therefore, we investigated the potential lipolytic effects of DLPC on adipocytes and insulin signaling in muscle cells. In this study, DLPC-treated 3T3-L1 adipocytes showed enhanced tumor necrosis factor α (TNF-α) release. Suppression of TNF-α by short interfering RNA (siRNA) mitigated DLPC-induced lipolysis and apoptosis. DLPC treatment increased peroxisome proliferator-activated receptor α (PPARα) expression levels in C2C12 myocytes. siRNA-mediated suppression of PPARα abrogated the suppressive effects of DLPC on palmitate-induced inflammation and insulin resistance. In conclusion, DLPC enhanced lipolysis and apoptosis via a TNFα-dependent pathway in adipocytes and attenuated palmitate-induced insulin resistance through PPARα-mediated suppression of inflammation in myocytes.

肥胖会导致胰岛素抵抗和2型糖尿病的发展。据报道磷脂酰胆碱（PPC）可以增加脂肪组织中的肝脏胰岛素敏感性和脂解作用，以解决局部肥胖症。在这项研究中，我们提出了1,2-二亚油酰基-snPPC的主要活性物质-glycero-3-phosphocholine（DLPC）是治疗肥胖症介导的疾病（例如脂肪代谢和胰岛素抵抗受损）的有效物质。因此，我们研究了DLPC对脂肪细胞和肌肉细胞中胰岛素信号传导的潜在脂解作用。在这项研究中，DLPC处理的3T3-L1脂肪细胞显示增强的肿瘤坏死因子α（TNF-α）释放。通过短干扰RNA（siRNA）抑制TNF-α可减轻DLPC诱导的脂解和细胞凋亡。DLPC处理可增加C2C12心肌细胞中过氧化物酶体增殖物激活受体α（PPARα）的表达水平。siRNA介导的PPARα抑制作用消除了DLPC对棕榈酸酯诱导的炎症和胰岛素抵抗的抑制作用。结论，