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神经节苷脂ＧＭ３诱导人单核样白血病Ｊ６－２细胞沿单核／巨噬细胞途径分化．在ＧＭ３诱导分化同时，Ｊ６－２细胞磷脂代谢发生了显著变化．采用（（３２）Ｐ）Ｐｉ、［ＧＨ３－３Ｈ］胆碱和［ＣＨ３－３Ｈ］ＳＡＭ参入实验对ＧＭ３影响Ｊ６－２细胞ＰＣ代谢的机制进行了初步的探讨．ＧＭ３促进［（３２）Ｐ］Ｐｉ参入Ｊ６－２细胞ＰＣ；抑制［ＣＨ３－３Ｈ］胆碱参入ＰＣ及ＰＣ合成的前体磷酸胆碱及ＣＤＰ－胆碱；ＧＭ３促进［ＣＨ３－３Ｈ］ＳＡＭ参入ＰＣ，但抑制［ＣＨ３－３Ｈ］ＳＡＭ参入ＰＣ合成的前体胆碱、磷酸胆碱和ＣＤＰ－胆碱．上述结果提示，ＧＭ３抑制Ｊ６－２细胞ＰＣ合成的ＣＤＰ－胆碱途径，促进ＰＣ合成的ＰＥ甲基化途径．
Ganglioside GM3 induces differentiation of human monocytic leukemia J6-2 cells along the monocyte/macrophage pathway. At the same time as GM3 induced differentiation, the phospholipid metabolism of J6-2 cells changed significantly. The ((32)P) Pi, [GH3-3H]choline and [CH3-3H]SAM incorporation experiments were used to investigate the mechanism of GM3 affecting PC metabolism in J6-2 cells. GM3 promotes [(32)P]Pi into J6-2 cell PC; inhibits [CH3-3H] choline incorporation into precursor PC and PC synthesis of phosphocholine and CDP-choline; GM3 promotes [CH3-3H] SAM incorporation PC, but inhibition of [CH3-3H]SAM incorporation into PC synthesis of precursors choline, phosphocholine, and CDP-choline. These results suggest that GM3 inhibits the CDP-choline pathway of PC synthesis in J6-2 cells and promotes the PE methylation pathway for PC synthesis.