Mastoparan(MAS) and α-latrotoxin(α-LTX) are two kinds of insulinotropic peptides obtained from insect toxins which can interact with islet β-cells and induce insulin secretion. The signal mechanism of these insulin...Mastoparan(MAS) and α-latrotoxin(α-LTX) are two kinds of insulinotropic peptides obtained from insect toxins which can interact with islet β-cells and induce insulin secretion. The signal mechanism of these insulinotropic peptides regulating insulin-releasing attracts notable attention and has been elucidated more and more details. MAS mainly acts on the molecular components of exocytosis at a late stage. Insulin secretion induced by MAS is obviously dependent on GTP,which subsequently activates G-protein located on insulin secretion granules(ISG),or activates the Rho subfamily of small G proteins to evoke exocytosis and sensitize fusion machinery. The MAS stimulated insulin-releasing activity can be augmented by nutrients. However,its effect is not Ca2+ dependent. There are two regulatory pathway triggered by α-LTX: one way is pore formation caused through plasma membrane,another way is the transmembrane signal transduction evoked by cytosolic second messengers. Tetrameri complexs assembled at high concentration of α-LTX toxin or in the presence of extracellular Ca2+,can insert α-LTX into plasma membrane to form Ca2+ permeable channels and trigger Ca2+-dependent secretion. By binding to transmembrane receptors and activating phospholipase C,α-LTX induces the generation of second messenger DAG and IP3. IP3 triggers Ca2+ influx and subsequently activates CaMK pathway,however,DAG also activates PKC pathway to increase insulin release.展开更多
文摘Mastoparan(MAS) and α-latrotoxin(α-LTX) are two kinds of insulinotropic peptides obtained from insect toxins which can interact with islet β-cells and induce insulin secretion. The signal mechanism of these insulinotropic peptides regulating insulin-releasing attracts notable attention and has been elucidated more and more details. MAS mainly acts on the molecular components of exocytosis at a late stage. Insulin secretion induced by MAS is obviously dependent on GTP,which subsequently activates G-protein located on insulin secretion granules(ISG),or activates the Rho subfamily of small G proteins to evoke exocytosis and sensitize fusion machinery. The MAS stimulated insulin-releasing activity can be augmented by nutrients. However,its effect is not Ca2+ dependent. There are two regulatory pathway triggered by α-LTX: one way is pore formation caused through plasma membrane,another way is the transmembrane signal transduction evoked by cytosolic second messengers. Tetrameri complexs assembled at high concentration of α-LTX toxin or in the presence of extracellular Ca2+,can insert α-LTX into plasma membrane to form Ca2+ permeable channels and trigger Ca2+-dependent secretion. By binding to transmembrane receptors and activating phospholipase C,α-LTX induces the generation of second messenger DAG and IP3. IP3 triggers Ca2+ influx and subsequently activates CaMK pathway,however,DAG also activates PKC pathway to increase insulin release.
