Numerous chemicals in the environment have the ability to interact with the endocrine system. These compounds are called endocrine disruptors (EDs).
Exposure to EDs represents one of the hypotheses for decreasing fertility, the increased risk of numerous cancers and obesity, metabolic syndrome and type 2 diabetes. There are various mechanisms of ED action, one of which is their interference in the action of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) that maintains a balance between active and inactive glucocorticoids on the intracellular level.
This enzyme has two isoforms and is expressed in various tissues. Inhibition of 11 beta HSD in various tissues can have different consequences.
In the case of EDs, the results of exposure are mainly adverse; on the other hand pharmaceutically developed inhibitors of 11 beta HSD type 1 are evaluated as an option for treating metabolic syndrome, as well as related diseases and depressive disorders. This review focuses on the effects of 11 beta HSD inhibitors in the testis, colon, adipose tissue, kidney, brain and placenta.