GCG and diabetes mellitus: Here we show that glucose-induced inhibition of KATP-channels in α cells results in inhibition of glucagon secretion, that the glucagon secretory defects associated with diabetes can be mimicked by experimental conditions leading to a tiny increase in KATP-channel activity, and that glucose-regulated glucagon secretion can be restored in diabetic or metabolically compromised islets by low concentrations of the KATP-channel blocker tolbutamide.