Prolonged stress has long been shown to have major effects on the
development of both type of diabetes mellitus, Type 1 and Type 2. Type 1
diabetes is an autoimmune disease that is characterized by the immune
system attacking self-antigens. There is a failure or breakdown in
immunological tolerance to allow this to happen. Prolonged physical or
emotional stress can activate the hypothalamus-pituitary-adrenal (HPA)
axis to induce production of the stress hormone glucocorticoid, causing
abrupt thymus involution and result in escape of autoreactive T- cells.
Though regulatory T-cells (Treg) are present in the circulation, they
are unable to suppress the autoreative T-cells from initiating the
destruction of β-cells and the subsequent development of Type 1
diabetes. Stress also causes metabolic disturbances, including altered
hepatic glucose metabolism, increased peripheral insulin resistance and
hyperglycemia. Glucocorticoid is the potential contributor to the
chronic hyperglycemia that results in insulin resistance and β-cell
dysfunction via the generation of oxidative stress which ultimately
leads to the development of Type 2 diabetes.