Mechanisms of glucocorticoid-induced insulin resistance: focus on adipose tissue function and lipid metabolism

Endocrinol Metab Clin North Am. 2014 Mar;43(1):75-102. doi: 10.1016/j.ecl.2013.10.005.


Glucocorticoids (GCs) are critical in the regulation of the stress response, inflammation and energy homeostasis. Excessive GC exposure results in whole-body insulin resistance, obesity, cardiovascular disease, and ultimately decreased survival, despite their potent anti-inflammatory effects. This apparent paradox may be explained by the complex actions of GCs on adipose tissue functionality. The wide prevalence of oral GC therapy makes their adverse systemic effects an important yet incompletely understood clinical problem. This article reviews the mechanisms by which supraphysiologic GC exposure promotes insulin resistance, focusing in particular on the effects on adipose tissue function and lipid metabolism.

Keywords: Adipose tissue; Cushing syndrome; Glucocorticoids; Insulin resistance; Lipids; Lipolysis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adipose Tissue / immunology
  • Adipose Tissue / metabolism
  • Adipose Tissue / physiology*
  • Glucocorticoids / adverse effects*
  • Glucocorticoids / immunology
  • Glucocorticoids / physiology*
  • Humans
  • Insulin Resistance / physiology*
  • Lipid Metabolism / physiology*


  • Glucocorticoids