Stress Hyperglycemia

Injury and destruction of the islets precede the onset of clinical hyperglycemia in Type 1 diabetes mellitus (DM). This represents the activation of an autoimmune state followed by an imbalance between T-helper and T-suppressor cells and the susceptibility or resistance of the β-cells to injury. Because some stress hormones (particularly cortisol) are known to modulate the immune system and others to alter islet β-cell activity (epinephrine, glucagon, cortisol), there has been speculation about the role of such modulation on the process of islet injury. Thus, neurohormonal changes associated with stress have been proposed as one of the environmental factors that interact with hereditary factors known to be associated with the risk of developing Type 1 diabetes.