“…After both a single dose and posterior 72 h of continuous treatment with carbenoxolone, in healthy male volunteers, Tomlinson et al observe a decrease not only on serum cortisol generation, after oral administration of cortisone acetate (although only significantly for continuous treatment), but also on cortisol concentrations, after oral cortisone acetate, and glycerol concentrations, after oral prednisone, both within SAT interstitial fluid (in the latter location being indicative of inhibition of GC-mediated lipolysis) . It is important to mention that 11-HSD2 inhibition, with licorice or carbenoxolone, can lead to cortisol-dependent mineralocorticoid excess, with hypertension, sodium retention, hypokalemia and fluid retention (Andrews et al, 2003;Edwards et al, 1988;Ferrari, 2010;Gathercole & Stewart, 2010;Palermo et al, 2004;Stewart et al, 1990;Stewart et al, 1987). 11 -HSD2 is expressed principally in the distal nephron, where it inactivates cortisol to cortisone and thereby protects MR from cortisol (Andrews et al, 2003;Edwards et al, 1988;Ferrari, 2010;Funder et al, 1988;Palermo et al, 2004).…”