胰岛素介体产生机制的探讨

胰岛素介体──肌醇磷酸多糖，被认为是胰岛素的第二信使，存在于细胞膜上的糖肌醇磷脂是产生该介体的前体，经胰岛素或磷脂酰肌醇特异性的磷脂酶Ｃ（ＰＩＰＬＣ）水解，产生介体和二酰甘油（ＤＧ）．本实验以人红细胞为材料，用３￣Ｈ同位素标记、有机溶剂提取、薄层层析及放射性自动计数等方法，分析胰岛素或ＰＩＰＬＣ作用于红细胞后前体和ＤＧ的变化情况，以推测介体的产生机制．结果显示：胰岛素使红细胞膜上及释放至胞外上清的前体量均较对照升高，且使体系中的ＤＧ量升高；ＰＩＰＬＣ则使红细胞膜上的前体量下降，使释放至胞外上清的前体量升高，推测：胰岛素或ＰＩＰＬＣ作用于完整细胞时，激活了某种酶，使前体先从膜上释放至胞外上清，再被水解为介体和ＤＧ，同时胰岛素还可能激活完整细胞内再合成前体的机制，而ＰＬＰＬＣ却不能．

A Study on the Mechanism of the Generation of Insulin Mediator

Insulin mediator,also called inositol phosphate glycan,mimics certain actions of insulin on metabolic enzymes. It has been considered as a“second messenger”of insulin and the most hopeful medicine to treat non-insulin-dependent diabetes mellitus (NIDDM) patients. The glycosyl-phosphatidylinositol of the cell membrane is the precursor from which the insulin mediator and diacylglycerol (DG)can be released by insulin or PIPLC. The precursor and DG were extracted from insulin or PIPLC treated , 3H-labelled human red blood cells by organic solvent extraction and separated on thin layer chromatography. The quantity of the precursor and DG were measured by digital autoradiography. The results showed; insulin could increase the quantity of precursors both on the cell membrane and in the supernatant. PIPLC could only increase the quantity of precursors released from the cell and decrease the quantity of membrane-bound precursors. Meanwhile both insulin and PIPLC could increase the quantity of DG in reactive system.It is proposed that before it is cleaved into mediator and DG,the precursor is first released from plasma membrane through activation of certain enzymes by insulin or PIPLC. Only insulin can activate the de novo synthesis mechanism of the precursor, PIPLC can not.