THE IMPACT OF SHORT AND MEDIUM-TERM GLUCOCORTICOID TREATMENT ON GLUCOSE HOMEOSTASIS .
RUCSANDRA DĂNCIULESCU MIULESCU¹, MĂDĂLINA MUŞAT^1*, CORINA NEAMŢU²
1-Carol Davila University of Medicine and Pharmacy, Bucharest
2-C.I. Parhon, Instit. Of Endocrinology, Bucharest
*-corresponding author: mdmusat@yahoo.com
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Abstract:

Glucocorticoids, like GH, are the main insulin-antagonistic hormones. They have various metabolic effects in the liver, adipose tissue, and muscle. In the liver, glucocorticoids serve as the key promoters of gluconeogenesis by activation of pyruvate carboxylase and phosphoenolpyruvate carboxykinase and stimulate hepatic uptake of amino acids and glycerol. At the level of adipose tissue and muscle, glucocorticoids antagonize the insulin-mediated uptake and the use of glucose. Glucocorticoids also exert a permissive effect on lipolysis by promoting the activation of cAMP-dependent hormone-sensitive lipase, a key enzyme inhibited by insulin. The net clinical effect of glucocorticoid excess in humans is a relocation of fat depots, which results in the typical central obesity of Cushing syndrome.
In healthy humans, short-term increments in plasma cortisol levels result in a slight increase in the levels of glucose, which is mediated by both hepatic and extrahepatic effects. However, the effects of chronic administration of moderate doses of glucocorticoids to healthy humans are usually compensated for by increased insulin release, which results in minimal changes in glucose levels. Thus, the spectrum of glucose intolerance in patients with Cushing syndrome or exogenous steroid use depends in large part on endogenous β-cell reserve, a situation similar to that in acromegaly.

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