basically glucose stimulates Beta cells to exocytose insulin. Any process involving exocytosis involves fusion of an intracellular vesicle with the plasma membrane.
basically glucose stimulates Beta cells to exocytos insulin. An process involving exocytosis involves fusion od an intracellular vesicle with the plasma membrane.
The β-cells have evolved a mechanism to detect the amount of insulin stored and secreted and adjust insulin synthesis accordingly. A granule transmembrane protein called islet cell autoantigen 512 (ICA512), is a crucial part of this feedback control. Insulin granules travel a long distance on tubulin tracks before arriving at the peripheral actin network . Before becoming linked to the cytoskeleton, insulin granules are anchored to actin cortex via ICA512 and β2-synthrophin. Upon activation, the granule membrane fuses transiently to the cell membrane to release insulin. Elevated Ca2+ levels in the meantime activate the protease μ-calpain to cleave away a cytosolic fragment from ICA512. The free ICA512 cytosolic fragment then moves to the nucleus and binds to the tyrosine-phosphorylated transcriptional factor STAT5 to prevent STAT 5 from dephosphorylation, which in turn upregulates insulin transcription . Nuclear free ICA512 cytosolic fragments also bind to sumoylating enzyme PIASγ. The sumoylation of ICA512 by PIAS γ reverses the binding of ICA512 to STAT5 . Hence, the release of insulin from secretory granules is communicated to the nucleus, which serves as a positive feedback mechanism to initiate insulin translation for maintaining an adequate amount of stored insulin.