FIG. 2.

Glucagon response in the presence and absence of an exogenous zinc switch-off signal during perifusion of STZ-induced diabetic wild-type mouse islets. Islets were pretreated with STZ to kill β-cells, thereby preventing endogenous insulin and zinc secretion. After an initial 30-min perifusion with 16.7 mmol/l glucose and zinc (Zn), at time 0 min the perifusate was changed. Glucagon levels increased significantly only when a perifusate containing no glucose and no zinc, which generated an exogenous zinc switch-off signal to α-cells during glucose deprivation, was begun at 0 min (■, n = 5). Glucagon secretion did not increase if at time 0 min only glucose, but not zinc, was switched off (○, n = 4) or if only zinc but not glucose was switched off (●, n = 4). If at time 0 min nifedipine (NIF) was added to the perifusate, glucagon secretion not only failed to rise but was suppressed despite the presence of the zinc switch-off signal during glucose deprivation (□, n = 3). ▴ at times −10 to 0 min represent the average of experimental values and control values.