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In this issue of Diabetes , Joy et al. (1) report that in healthy individuals hyperinsulinemic hypoglycemia, compared with hyperinsulinemic euglycemia, reduced endogenous nitric oxide (NO)-mediated endothelial vasodilation, activated inflammatory processes, impaired fibrinolytic balance, and increased proatherothrombotic mechanisms and that repeated episodes of hypoglycemia on two consecutive days further impaired vascular function by additionally reducing both endogenous and exogenous NO-mediated endothelial function. Because the data during both day one and day two hyperinsulinemic-hypoglycemic clamps were contrasted with day one hyperinsulinemic-euglycemic clamps, the data implicate hypoglycemia, rather than hyperinsulinemia, in the development of these responses. However, their mechanisms, particularly any relationship with the documented sympathoadrenal responses to hypoglycemia and the attenuated sympathoadrenal responses to hypoglycemia following recent antecedent hypoglycemia (2,3), were not determined. These translational data support the notion that iatrogenic hypoglycemia may contribute to the pathogenesis of atherosclerotic vascular disease in diabetes (4,5) and extend that to include a further effect of recurrent hypoglycemia.Iatrogenic hypoglycemia causes recurrent morbidity in most people with type 1 diabetes and many …

Hypoglycemia-Associated Autonomic Failure in Diabetes: Maladaptive, Adaptive, or Both?