This metabolic effect of the ACE inhibition is probably not due to the reduced synthesis of angiotensin II, but to the inhibition of the degradation of bradykinins and an improved blood circulation of the skeletal muscles. Kinins and the prostaglandins they produce have been shown to improve insulin activity. Angiotensin II shows no metabolic effects in the periphery. ACE inhibition is associated with a reduction in insulin resistance. The disorders of the metabolic syndrome are not intensified, the insulin requirement - hyperinsulinemia - is not increased.