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Pancreatic β-cell insulin secretion, which responds to various secretagogues and hormonal regulations, is reviewed here, emphasizing the fundamental redox signaling by NADPH oxidase 4- (NOX4-) mediated H 2 O 2 production for glucose-stimulated insulin secretion (GSIS). There is a logical summation that integrates both metabolic plus redox homeostasis because the ATP-sensitive K + channel (K ATP ) can only be closed when both ATP and H 2 O 2 are elevated. Otherwise ATP would block K ATP , while H 2 O 2 would activate any of the redox-sensitive nonspecific calcium channels (NSCCs), such as TRPM2. Notably, a 100%-closed K ATP ensemble is insufficient to reach the -50 mV threshold plasma membrane depolarization required for the activation of voltage-dependent Ca 2+ channels. Open synergic NSCCs or Cl - channels have to act simultaneously to reach this threshold. The resulting intermittent cytosolic Ca 2+ -increases lead to the pulsatile exocytosis of insulin granule vesicles (IGVs). The incretin (e.g., GLP-1) amplification of GSIS stems from receptor signaling leading to activating the phosphorylation of TRPM channels and effects on other channels to intensify integral Ca 2+ -influx (fortified by endoplasmic reticulum Ca 2+ ). ATP plus H 2 O 2 are also required for branched-chain ketoacids (BCKAs); and partly for fatty acids (FAs) to secrete insulin, while BCKA or FA β-oxidation provide redox signaling from mitochondria, which proceeds by H 2 O 2 diffusion or hypothetical SH relay via peroxiredoxin "redox kiss" to target proteins.

The Pancreatic β-Cell: The Perfect Redox System