Mechanisms of Glucocorticoid-Induced Insulin Resistance

✍ Scribed by Geer, Eliza B.; Islam, Julie; Buettner, Christoph

• Book ID: 121779615
• Publisher: Elsevier Science
• Year: 2014
• Tongue: English
• Weight: 639 KB
• Volume: 43
• Category: Article
• ISSN: 0889-8529
• DOI: 10.1016/j.ecl.2013.10.005

✦ Synopsis

Glucocorticoids (GCs) are critical in the regulation of energy homeostasis. GCs liberate energy substrates during stress by enhancing muscle protein breakdown, adipose tissue lipolysis, hepatic gluconeogenesis, and reducing glucose utilization, all of which elevate circulating glucose concentrations. Chronic excessive GC exposure results in whole-body insulin resistance and the development of abdominal adiposity in humans. The ability of GCs to induce adipose tissue lipolysis depends on their concentration, duration of exposure, and the specific adipose tissue depot. 11b-Hydroxysteroid dehydrogenase 1 is a gatekeeper for intracellular GC availability through the local activation of GCs within tissues. Prevalent forms of subtle GC excess include exogenous exposure as treatment of autoimmune and rheumatologic diseases, or chronic stress with resultant activation of the hypothalamic-pituitary-adrenal axis.