Overexpression of 11 beta-Hydroxysteroid Dehydrogenase Type 1 in Hepatic and Visceral Adipose Tissue is Associated with Metabolic Disorders in Morbidly Obese Patients

The enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1) catalyzes intracellular glucocorticoid reactivation by conversion of cortisone to cortisol in different tissues and have been implicated in several metabolic disorders associated with obesity. The aim of this study was to evaluate the 11 beta-HSD1 expression in liver, visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) in morbidly obese patients undergoing bariatric surgery and its correlations with clinical, anthropometric, and biochemical variables. A prospective study was conducted over a 27-month period. Hepatic, VAT, and SAT samples were obtained at the time of surgery. 11 beta-HSD1 and 18S gene expression was measured using real-time quantitative reverse transcriptase-polymerase chain reaction. Forty nine patients met the inclusion criteria [mean age: 42.2 +/- 10 years, body mass index (BMI): 42 +/- 6 kg/m(2), 71% women and 63% with metabolic syndrome (MS)]. 11 beta-HSD1 mRNA levels were higher in liver than fat tissue (p < 0.001), being higher in SAT than in VAT (p < 0.001) without gender-specific differences. Hepatic expression of 11 beta-HSD1 correlated positively with SAT and VAT, alanine aminotransferase (ALT), and serum glucose and was inversely associated with BMI. 11 beta-HSD1 mRNA in VAT correlated positively with insulinemia, ALT, and LDL cholesterol. There were no associations between 11 beta-HSD1 mRNA in SAT and the variables analyzed. 11 beta-HSD1 expression is higher in liver in comparison to adipose tissue in obese patients. The observed correlations between hepatic and VAT 11 beta-HSD1 expression with dyslipidemia and insulin resistance suggest that this enzyme might have a pathogenic role in obesity and related metabolic disorders.