LacZ L, cells infected with ade-LacZ grow in HBSS buffer with 3mM glucose LacZ H, cells infected with ade-LacZ grow in HBSS buffer with 15mM glucose Del L, cells infected with ade-del grow in HBSS buffer with 3mM glucose Del H, cells infected with ade-del grow in HBSS buffer with 15mM glucose Supernatant for GSIS samples, then lysis cell for testing insulin content.

Figure 2. Structural components (italicized) of the pancreatic  -cell involved in glucose-induced biosynthesis and release of insulin. Glucose Transport of proinsulin to Golgi 3 vesicles Transfer Synthesis of preproinsulin; Excision of signal peptide; Disulfide bonds formed 2 Endoplasmic reticulum Microfilaments Nucleus mRNA production; Preproinsulin gene transcription 1 Golgi Proinsulin to insulin; Packaging of insulin 4 Insulin storage 5 Microtubules Secretory granules Ca 2+ contraction Of microfilaments Granule fusion with membrane; Exocytosis of insulin 7 Ca 2+ Biological structures

The defining property of KATP channels is the inhibition by intracellular ATP. KATP channels are octamers composed of four pore forming a -subunits (the inward rectifier channels Kir6.1 or Ki6.2) and four regulatory b -subunits (the sulphonylurea receptors SUR1 or SUR2. * My real-time PCR results proved sur.1 and sur6.2 RNA level in cells treated with ade-del C perk down 50%-25% compared to ade-LacZ. KATP channels are regulated by intracellular pH (24), protein kinase A (25,26) and protein kinase C. In addition, phosphatidylinositol 4,5 bisphosphate (PIP2), a membrane-bound phospholipid involved in G-protein-mediated signal transduction, can activate KATP channels.