two isoenzymes associated with the interconversion of cortisol and cortisone. In the kidney and placenta, reaction is toward cortisone (enzyme type 2) that is inactive as both a glucocorticoid and a mineralocorticoid. This protects the fetus from cortisol-induced salt retention and from the mother's glucocorticoid. Congenital or pharmacologically induced deficiency of this enzyme causes hypertension and electrolyte abnormalities. In liver and adipose tissue, reaction is toward cortisol (enzyme type 1) that is active as both a glucocorticoid and a mineralocorticoid. Knock-out of the gene that codes for this enzyme protects experimental animals from obesity.
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Examples: glitazone, GI cocktail, etc.