Characterisation of 11β-hydroxysteroid dehydrogenase 1 in human orbital adipose tissue: a comparison with subcutaneous and omental fat

Abstract

Abstract Glucocorticoids (GCs) have a profound effect on adipose biology increasing tissue mass causing central obesity. The prereceptor regulation of GCs by 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1) that activates cortisol from cortisone has been postulated as a fundamental mechanism underlying the metabolic syndrome mediating adipocyte hyperplasia and hypertrophy in the omental (OM) depot. Orbital adipose tissue (OF) is the site of intense inflammation and tissue remodelling in several orbital inflammatory disease states. In this study, we describe features of the GC metabolic pathways in normal human OF depot and compare it with subcutaneous (SC) and OM depots. Using an automated histological characterisation technique, OF adipocytes were found to be significantly smaller (parameters: area, maximum diameter and perimeter) than OM OF harbours a large CD68 C population. These characteristics define an orbital microenvironment that has the potential to respond to sight-threatening orbital inflammatory disease