[Improved insulin action by ACE inhibition in type-2 diabetics]

The effect of the angiotensin converting enzyme inhibitor captopril (25 mg by mouth) on glucose metabolism of skeletal muscle and the whole organism was studied in nine normotensive type II (non-insulin dependent) diabetics using a combination of euglycaemic-hyperinsulinaemic glucose-clamp and forearm catheter techniques. The administration of captopril resulted in a significant rise of both the whole-body glucose elimination and utilization rate in the forearm musculature. At the same time the arterial kinin level rose, while the concentrations of insulin, free fatty acids and gluconeogenesis precursors, as well as the number and activity of insulin receptors (measured in an erythrocyte-binding study) remained unchanged. The data support the view that, in type II diabetics, ACE inhibition raises the insulin-stimulated glucose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature. The demonstration of an increased kinin level points to this effect possibly being caused by the reduced breakdown of locally liberated kinins.