Effect of acute hyperglycaemia on plasma potassium and aldosterone levels in type 2 (non-insulin-dependent) diabetes.

Abstract

Potassium homeostasis during a 50-g oral glucose tolerance test was studied in 14 newly diagnosed, untreated Type 2 (non-insulin-dependent) diabetics. They showed a rise in plasma potassium from a mean +/- SEM basal of 3.9 +/- 0.1 to 4.4 +/- 0.1 mmol/l at 60 min and to 4.6 +/- 0.1 mmol/l at 90 min (p less than 0.01), whereas no change was seen in a group of 14 normal subjects. A possible role of mineralocorticoids was sought by measuring simultaneous serum aldosterone and deoxycorticosterone levels. Aldosterone was reduced after the glucose load in all subjects studied, falling to 73% of basal at 60 min in diabetics (p less than 0.01), and to 61% of basal at 90 min in normal subjects (p less than 0.001). Serum deoxycorticosterone showed a similar pattern. Thus it is unlikely that the rise in plasma potassium seen in the diabetic patients was due to abnormal levels of mineralocorticoids. Since the diabetic subjects were found to have an intact insulin response to the glucose load, it is suggested that resistance to insulin-stimulated potassium uptake into cells might be involved in the pathogenesis of the paradoxical hyperkalaemia induced by acute hyperglycaemia.