Zhang Yuebo, Huang Cheng, Sheng Xiaoyan, Gong Zhenwei, Zang Ying Qin
Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Graduate School of CAS, Chinese Academy of Sciences, Shanghai, 200031, PR China.
Int J Mol Med. 2009 Apr;23(4):449-54.
Lecithin is an essential biological component and widely used as a nutritional supplement for protecting cells from oxidation, increase fat burning and preventing cardiovascular disease. Lecithin contains fatty acids identified as the peroxisome proliferator-activated receptor (PPAR) agonists. However, the role of lecithin in adipogenesis and lipogenesis remains elusive. 3T3-L1 cells and mouse primary preadipocytes were used to characterize the properties of lecithin related to adipogenesis and lipogenesis. We found that lecithin promoted adipocyte differentiation and differentiation-specific gene expression, and increased triglycerides and free fatty acid levels in the adipocytes. These effects are independent of the clonal expansion of 3T3-L1 cells and the upstream PPARgamma regulator, CCAAT-enhancer-binding protein beta. Furthermore, lecithin induced lipid accumulation in human hepatoma HepG2 cells. Our data suggest that lecithin is involved in adipogenesis, lipogenesis and hepatic lipid accumulation and it is implicated in obesity and hepatic steatosis.
卵磷脂是一种重要的生物成分，被广泛用作营养补充剂，用于保护细胞免受氧化、增加脂肪燃烧和预防心血管疾病。卵磷脂含有被鉴定为过氧化物酶体增殖物激活受体（PPAR）激动剂的脂肪酸。然而，卵磷脂在脂肪生成和脂质生成中的作用仍不清楚。使用3T3-L1细胞和小鼠原代前脂肪细胞来表征与脂肪生成和脂质生成相关的卵磷脂特性。我们发现卵磷脂促进脂肪细胞分化和分化特异性基因表达，并增加脂肪细胞中的甘油三酯和游离脂肪酸水平。这些作用独立于3T3-L1细胞的克隆扩增和上游PPARγ调节因子CCAAT增强子结合蛋白β。此外，卵磷脂诱导人肝癌HepG2细胞中的脂质积累。我们的数据表明，卵磷脂参与脂肪生成、脂质生成和肝脏脂质积累，与肥胖和肝脂肪变性有关。
