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Expression of somatostatin receptor subtypes 1–5 in pancreatic islets of normoglycaemic and diabetic NOD mice

¹ Departments of Medical Cell Biology and ² Medical Sciences, Uppsala University, Uppsala, Sweden

(Correspondence should be addressed to E Ludvigsen, Department of Medical Cell Biology Husargatan 3, Box 571 SE-75123 Uppsala, Sweden; Email: Eva.Ludvigsen{at}medcellbiol.uu.se)

Objective: Somatostatin acts on five specific receptors (sst1–5) to elicit different biological functions. The non-obese diabetic (NOD) mouse is an experimental model of type 1 diabetes. The aim of this study was to investigate whether the islet expression of sst1–5 is affected during the development of diabetes in NOD mice, with insulitis accompanied by spontaneous hyperglycaemia.

Methods: By immunostaining for sst1–5 the expression and co-expression together with the four major islet hormones in pancreatic islets were investigated in female and male NOD mice at different stages of disease. The NOD related non-diabetic ICR mouse was also examined.

Results: The islet cells of diabetic NOD mice showed an increased islet cell expression of sst2–5 compared with normoglycaemic female NOD mice. This correlated to increasing age and extent of insulitis. Major findings from the co-expression investigations were that sst2 was expressed in a majority of ß-cells in the normoglycaemic NOD mice, but absent in the ß-cells in the diabetic NOD mice. A majority of the -cells expressed sst2 and 5 in normoglycaemic and diabetic NOD mice. About 60% of -cells showed co-expression of sst4 and 5 in both normoglycaemic and diabetic NOD mice. 60% of pancreatic polypeptide (PP)-cells expressed sst4 in both groups. Insulitis was found to be accompanied by a down-regulation of sst in normoglycaemic animals.

Conclusions: The difference in sst expression in the islets cells of diabetic mice may suggest either a contributing factor in the process leading to diabetes, or a defence response against ongoing ß-cell destruction.