11 Beta HSD type 1 is responsible for low plasma HDL-cholesterol and abdominal obesity in metabolic syndrome patients
11ß-hydroxysteroid dehydrogenase (11ß-HSD) isozymes regulate the access of glucocorticoids (GCs) to their receptors and catalyze the interconvension of active glucocorticoids to their inactive metabolites. 11ß-HSD type 1 is expressed in liver, brain, lung and adipose tissues but has not been reported to be present in human epicardial adipose and aorta tissues. 11ß-HSD expression plays an essential role in abdominal obesity which is one of the major causes of metabolic syndrome. We have investigated the role of 11 ß-HSD type 1 in paired biopsies from epicardial adipose and aorta tissues of 10 obese metabolic syndrome patients (median age,61.30yrs; median BMI,29.57kg/m2, waist hip ratio,47.38) undergoing coronary artery by pass graft operation. The mRNA level of 11 ß-HSD type 1 was assessed in whole tissue using the real time- PCR. We have observed that human epicardial tissues and human aorta tissues express mRNA for the Type I isoform and in human epicadial and aortic tissues. In aorta tissue, mRNA of 11ß-HSD Type 1 isoform levels did have a positive correlation with waist hip ratio (r=0.579;P<0.05) whereas showed negative correlation with hypertension (r=-0.543; P<0.05). In epicardial tissue, mRNA of 11ß-HSD Type 1 isoform showed negative correlation with HDL (r=-0.614; P< 0.05).
The analysis indicate that 11ß-HSD mRNA levels were related to waist-hip ratio and low plasma HDL-cholesterol of our patients, but did not show any correlation with coronary arthery disease. Besides, 11ß-HSD showed a negative correlation with hypertansion which would indicate its regulatory role in blood pressure.
The outcome of this study show that 11ß-HSD might be responsible for Metabolic syndrome without hypertension.