Figure 1
Schematic model for glucose-dependent regulation of glucagon secretion in the mouse α-cell. Glucose is incorporated into the
α-cell by the transporter SLC2A1. At low-glucose concentrations, the moderate activity of KATP channels situates the α-cell membrane potential in a range that allows the opening of voltage-dependent T- and N-type Ca2+ channels and voltage-dependent Na+ channels. Their activation triggers action potentials, Ca2+ influx and exocytosis of glucagon granules. The opening of A-type K+ channels is necessary for action potential repolarization. However, high-glucose concentrations elevate the intracellular
ATP/ADP ratio, blocking KATP channels and depolarizing the membrane potential to a range where the inactivation of voltage-dependent channels takes place.
This results in the inhibition of electrical activity, Ca2+ influx and glucagon secretion. The function of L-type channels predominates when cAMP levels are elevated. See text for further
details.