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In adipose tissue, AKR1C3 is co\u2010expressed with 11\u03b2\u2010hydroxysteroid dehydrogenase type 1 (HSD11B1), which catalyzes not only the local activation of glucocorticoids but also the inactivation of 11\u2010oxygenated androgens, and thus has the potential to counteract AKR1C3. Using a combination of in\u00a0vitro assays and in silico modeling we show that HSD11B1 attenuates the biosynthesis of the potent 11\u2010oxygenated androgen, 11\u2010ketotestosterone (11KT), by AKR1C3. Employing ex\u00a0vivo incubations of human female adipose tissue samples we show that inhibition of HSD11B1 results in the increased peripheral biosynthesis of 11KT. Moreover, circulating 11KT increased 2\u20133 fold in individuals with type 2 diabetes after receiving the selective oral HSD11B1 inhibitor AZD4017 for 35\u2009days, thus confirming that HSD11B1 inhibition results in systemic increases in 11KT concentrations. 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