Glucocorticoids play an important role in determining adipose tissue metabolism and distribution. Patients with
Cushing's syndrome or receiving
corticosteroid therapy develop a reversible
visceral obesity. In obese patients, although circulating concentrations of
cortisol are not consistently elevated, local conversion of inactive
cortisone to active
cortisol in adipose tissue, catalyzed by
11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1), could amplify
glucocorticoid signaling. We have studied, using semiquantitative in situ hybridization, 11beta-HSD-1
mRNA expression in the adipocyte and stromal compartments of sc abdominal adipose tissue obtained from 12 lean patients and sc abdominal and visceral adipose tissue obtained from 18 obese patients. 11beta-HSD-1
mRNA was expressed in adipocytes, stroma, and walls of vessels. Localization of 11beta-HSD-1
mRNA did not differ between lean sc and obese sc or visceral adipose tissue. 11beta-HSD-1
mRNA levels were significantly (P = 0.0106) increased in the adipocyte compartment of sc adipose tissue obtained from obese patients as compared with nonobese ones, whereas no significant change (P = 0.446) was found in the stromal compartment. In obese patients, 11beta-HSD-1
mRNA expression was increased (P = 0.0157) in the stromal compartment of visceral compared with sc tissue, whereas no significant change (P = 0.8767) was found in the adipocyte compartment. In summary, our data show that 11beta-HSD-1
mRNA is increased in adipose tissue from obese patients, in the abdominal sc fat in adipocytes and in the visceral fat in both adipocytes and stroma. This observation suggests that an overexpression of 11beta-HSD-1 may explain part of the
glucocorticoid-induced metabolic disorders linked to
obesity and may promote visceral fat deposition.