ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2007) 13 P160

Immunohistochemical localisation of 11β-hydroxysteroid dehydrogenase type 1 in murine pancreatic islets

Angie Swali, Elizabeth Walker, Jeremy Tomlinson & Paul Stewart


The University of Birmingham, Birmingham, United Kingdom.


The metabolic syndrome, which encompasses features of obesity, insulin resistance, dyslipidaemia and hypertension, has been associated with excessive glucocorticoid (GC) exposure. The pancreas is a target of the adverse affects of GC action, resulting in β-cell damage and reduced glucose-stimulated insulin secretion (GSIS). 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyses the in vivo conversion of inactive to active glucocorticoids (cortisone E/11-dehydrocorticosterone A to cortisol F/corticosterone B); NADPH-dependent oxo-reductase activity facilitates cortisol to the glucocorticoid receptor (GR). The aim of this study was to investigate the presence and specific location of 11β-HSD1 within murine pancreatic islets. Serial sections through the pancreas of male and female C57BL/6 mice (n=6) were stained by immunohistochemistry to characterise the pattern of the main pancreatic hormones (insulin, glucagon, somatostatin (SS) and pancreatic polypeptide (PP)), GR and 11β-HSD1. The pattern of staining was further investigated with immunofluorescence to detect co-localisation of 11β-HSD1 with each of the pancreatic hormones (n=3). All pancreatic hormones were identified specifically within the pancreatic islets. While insulin was located within the core of the islet, the other hormones were found around the periphery of islets. 11β-HSD1 was also confined to the periphery with a pattern most similar to that of glucagon. GR staining occurred throughout the islet, but more densely in the exocrine tissue. Immunofluorescence revealed that 11β-HSD1 was not co-localised with insulin as previously reported in rodent islets, but instead with glucagon and PP-producing cells. These findings are the first to localise 11β-HSD1 to the alpha cell and highlight the potential role of 11β-HSD1 mediated control of glucagon secretion. This knowledge adds insight into the pathway by which this important enzyme could activate GCs within the endocrine pancreas, causing local manifestations of GC excess. This study is important in understanding the autocrine control of GCs within the normal pancreas, their role in GSIS and identification of possible candidates in the pathogenesis of Type 2 Diabetes Mellitus.

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