Abstract
The fact that obesity is a prominent feature of Cushing’s syndrome (systemic hypercortisolism
of adrenocortical origin) stimulated a 40-year search for evidence of systemic hypercortisolism
in human obesity. That search has failed to find such evidence. For the past 15 years,
however, studies have been done to evaluate a possible alternative type of hypercortisolism
in obesity, namely visceral adipose tissue (VAT) intracellular hypercortisolism. The
current review summarizes the evidence published so far about this possibility. There
have been three types of evidence studied: direct measurement of the VAT levels of
11β-hydroxysteroid dehydrogenase type I (11-HSD-1), which converts biologically inactive
cortisone to biologically active cortisol; direct measurement of splanchnic cortisol
production; and evaluation of the effect of a specific inhibitor of 11-HSD-1 on metabolic
abnormalities associated with obesity, particularly diabetes mellitus. The results
are complex and difficult to interpret. Our conclusion is that the presence of VAT
intracellular hypercortisolism in human obesity is possible but unlikely.
Key words
obesity - intracellular cortisol production - 11β-hydroxysteroid dehydrogenase
