Phosphatidylethanolamine N-methyltransferase (PEMT) is a small integral membrane protein that converts phosphatidylethanolamine (PE) into phosphatidylcholine (PC). It has been previously reported that, unexpectedly, PEMT deficiency protected from high-fat diet (HFD)-induced obesity and insulin resistance, pointing to a possible role of this enzyme in the regulation of adipose cell metabolism. Using mouse 3T3-L1 preadipocytes as a biological system, we demonstrate that PEMT expression is strongly increased during the differentiation of preadipocytes into mature adipose cells. Knockdown of PEMT reduced the expression of early and late adipogenic markers, inhibited lipid droplet formation, reduced triacylglycerol content and decreased the levels of leptin release from the adipocytes, suggesting that PEMT is a novel and relevant regulator of adipogenesis. Investigation into the mechanisms whereby PEMT regulates adipocyte differentiation revealed that extracellularly regulated kinases (ERK1/2) and AKT are essential factors in this process. Specifically, the activities of ERK1/2 and AKT, which are decreased during adipocyte differentiation, were elevated upon Pemt knockdown. Moreover, treatment of cells with exogenous ceramide 1-phosphate (C1P), which we reported to be a negative regulator of adipogenesis, decreased PEMT expression, suggesting that PEMT is also a relevant factor in the anti-adipogenic action of C1P. Altogether, the data presented here identify PEMT as a novel regulator of adipogenesis and a mediator of the anti-adipogenic action of C1P.

磷脂酰乙醇胺N-甲基转移酶（PEMT）是一种小的完整膜蛋白，可将磷脂酰乙醇胺（PE）转换为磷脂酰胆碱（PC）。先前已报道，出乎意料的是，PEMT缺乏症可防止高脂饮食（HFD）引起的肥胖症和胰岛素抵抗，这表明该酶可能在调节脂肪细胞代谢中发挥作用。使用小鼠3T3-L1前脂肪细胞作为生物系统，我们证明了PEMT表达在前脂肪细胞分化为成熟脂肪细胞的过程中强烈增加。剔除PEMT可减少早期和晚期脂肪形成标记的表达，抑制脂质滴形成，降低三酰甘油含量，并降低脂肪细胞中瘦素的释放水平，这表明PEMT是一种新型且相关的脂肪形成调节剂。对PEMT调节脂肪细胞分化的机制的研究表明，细胞外调节激酶（ERK1 / 2）和AKT是该过程中的重要因素。具体来说，在脂肪细胞分化过程中降低的ERK1 / 2和AKT活性在Pemt组合式。此外，用我们报道为脂肪形成的负调节剂的外源性神经酰胺1-磷酸（C1P）处理细胞会降低PEMT表达，这表明PEMT也是C1P抗脂肪形成作用的相关因素。总之，此处提供的数据将PEMT鉴定为脂肪形成的新型调节剂和C1P抗脂肪形成作用的介质。