Glucagon-induced increase in plasma potassium levels in type 1 (insulin-dependent) diabetic subjects

To investigate the hypothesis that in Type 1 (insulin-dependent) diabetes the increase in plasma potassium during decompensation may be due to a rise in glucagon concentrations, we have measured plasma glucose, potassium and glucagon levels in five diabetic patients during two tests with 0.154 mol/l saline or somatostatin (500 micrograms/h) performed on two successive days. The patients were maintained normoglycaemic overnight by means of a continuous insulin infusion. After insulin withdrawal during the saline infusion, glucose and potassium levels rose markedly (delta maximum: glucose, 12.0 +/- 1.5 mmol/l; potassium, 0.73 +/- 0.12 mmol/l), while glucagon showed a slight, but significant increment (delta maximum: 10.6 +/- 1.0 pmol/ml, p less than 0.05). The potassium increment was not mediated by a reduction in blood pH. Somatostatin abolished the rise in glucagon concentration and simultaneously markedly inhibited the rise in potassium and glucose levels. It is concluded that in acute insulin deficiency, glucagon could be one of the factors that contributes to hyperkalaemia.