11β-Hydroxysteroid Dehydrogenase Type 1 is Overexpressed in Subcutaneous Adipose Tissue of Morbidly Obese Patients
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11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme catalyzes interconversion of inactive cortisone to active cortisol. Its expression in adipose tissue has been associated with obesity and some of its metabolic disorders. Controversies regarding which fat depots [subcutaneous adipose tissue (SAT) or visceral adipose tissue (VAT)] have higher expression still remain. The aim of this work was to evaluate 11β-HSD1 expression in SAT and VAT of obese patients and evaluate its association to metabolic features of metabolic syndrome.
In 32 morbidly obese patients, paired samples of SAT and VAT were collected. All patients, 40.2 ± 12.3 years and 36.7 ± 3.8 body mass index (BMI), underwent sleeve gastrectomy or laparoscopic gastric bypass. Gene expression of 11β-HSD1 in adipose tissue samples were determined by real-time reverse transcriptase polymerase chain reaction. Spearman correlation test was used to evaluate relationships between 11β-HSD1 levels and clinical and biochemical parameters.
11β-HSD1 mRNA levels were higher in SAT than in VAT, with median expression levels of 11.4 arbitrary units (AU) and 7.8 AU, respectively (p = 0.03). SAT 11β-HSD1 mRNA were correlated with VAT mRNA levels (r = −0.6, p = 0.018) and hip circumference (r = 0.66, p = 0.018). SAT 11β-HSD1 levels increase parallel according to BMI category. We did not find a correlation between SAT or VAT with fasting glucose (r = 0.15, p = NS), total cholesterol (r = 0.13, p = NS), triglycerides (r = 0.04, p = NS), and high-density lipoprotein (r = −0.16, p = NS). However, SAT expression in patients with features of MS was higher than those without features of MS.
Our results demonstrate that SATs express higher 11β-HSD1 mRNA levels than VAT. This finding highlights the importance of SAT in obesity and its possible role on metabolic disorders associated with obesity.
KeywordsAdipose tissue 11β-Hydroxysteroid dehydrogenase type 1 Morbid obesity Glucocorticoid Cortisol
This work was supported by Chilean grant FONDECYT 1070876. Dr. Muñoz’s scholarship is funded by MECESUP and Faculty of Medicine, Pontificia Universidad Católica de Chile.