Expression and Activity of 11 beta-Hydroxysteroid Dehydrogenase Type 1 Enzyme in Subcutaneous and Visceral Adipose Tissue of Prepubertal Children

Background: Glucocorticoid excess promotes visceral obesity and cardiovascular disease. Ligand availability to the glucocorticoid receptor is controlled by isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) which converts endogenous cortisone to active cortisol. Aim: To evaluate the expression and activity of 11 beta-HSD1 in subcutaneous adipose tissue (SC) and visceral adipose tissue (VAT) in prepubertal children with normal weight. Methods: Fourteen patients (11 female/3 male) with a mean age of 6.9 +/- 0.9 years and a body mass index (BMI) of 17.4 +/- 0.61 underwent elective open abdominal surgery. Results: Expression of 11 beta-HSD1 mRNA in SC and VAT was similar (0.8 +/- 0.15 vs. 0.61 +/- 0.12 AU). The activity of this enzyme in SC was significantly lower compared to VAT (1.42 +/- 0.39 vs. 2.79 +/- 0.61 ng cortisol/g tissue/24 h, p < 0.05). In addition, we observed a significant direct correlation with the expression of 11 beta-HSD1 in VAT adipose tissue with the patient's BMI (r = 0.825, p = 0.002). Conclusions: This correlation together with the increased activity of this enzyme in visceral adipose tissue might contribute to decreased hepatic insulin sensitivity due to increased portal cortisol when BMI increases. These observations appear to be particularly important in children born with low birth weight who develop rapid early weight gain. Copyright (C) 2009 S. Karger AG, Basel