[Glucocorticoid-induced insulin resistance and diabetes mellitus. Receptor-, postreceptor mechanisms, local cortisol action, and new aspects of antidiabetic therapy]

Med Klin (Munich). 2003 Apr 25;98(5):266-70. doi: 10.1007/s00063-003-1255-z.
[Article in German]

Abstract

Background: Glucocorticoids are frequently prescribed drugs. Nearly half of the patients treated with glucocorticoids over a longer period develop a deranged glucose metabolism. In about 50%, these disturbances persist despite reduction or even withdrawal of the drug.

Pathophysiology: Glucocorticoids antagonize the insulin-mediated inhibition of hepatic glucose release, decrease glucose utilisation in muscle, and reduce the binding affinity of insulin receptors. Therefore, glucocorticoid-induced diabetes mellitus is equivalent to unmasked type 2 diabetes. New studies presume that an increased endogenous production of glucocorticoids particularly in adipocytes could play a role in type 2 diabetes as well.

Therapy: Patients with glucocorticoid-induced diabetes bear, comparable to patients with other types of diabetes, a considerable risk of arteriosclerotic and cardiovascular diseases and should therefore receive an intensified treatment. Therapy of glucocorticoid-induced diabetes basically corresponds to that of type 2 diabetes. Applicable are oral antidiabetic drugs, particularly metformin and the glitazones as insulin sensitizers both requiring consideration of contraindications, or treatment with insulin.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / chemically induced*
  • Diabetes Mellitus, Type 2 / drug therapy
  • Gene Expression Regulation / drug effects
  • Glucocorticoids / administration & dosage
  • Glucocorticoids / adverse effects*
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Insulin Resistance* / physiology
  • Receptors, Glucocorticoid / drug effects*
  • Receptors, Glucocorticoid / genetics

Substances

  • Glucocorticoids
  • Hypoglycemic Agents
  • Receptors, Glucocorticoid