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Subtype selective interactions of somatostatin and somatostatin analogs with sst1, sst2 and sst5 in BON-1 cells
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
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2004 In: Medical Oncology, ISSN 1357-0560, Vol. 21, no 3, 285-295 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2004. Vol. 21, no 3, 285-295 p.
URN: urn:nbn:se:uu:diva-93889OAI: oai:DiVA.org:uu-93889DiVA: diva2:167520
Available from: 2006-01-13 Created: 2006-01-13Bibliographically approved
In thesis
1. Somatostatin Receptor Expression and Biological Functions in Endocrine Pancreatic Cells
Open this publication in new window or tab >>Somatostatin Receptor Expression and Biological Functions in Endocrine Pancreatic Cells
2006 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Type 1 diabetes is resulting from the selective destruction of insulin-producing beta-cells within the pancreatic islets. Somatostatin acts as an inhibitor of hormone secretion through specific receptors (sst1-5).

All ssts were expressed in normal rat and mouse pancreatic islets, although the expression intensity and the co-expression pattern varied between ssts as well as between species. This may reflect a difference in response to somatostatin in islet cells of the two species.

The Non-Obese Diabetic (NOD) mouse model is an experimental model of type 1 diabetes, with insulitis accompanied by spontaneous hyperglycaemia. Pancreatic specimens from NOD mice at different age and stage of disease were stained for ssts. The islet cells of diabetic NOD mice showed increased islet expression of sst2-5 compared to normoglycemic NOD mice. The increase in sst2-5 expression in the islets cells may suggest either a contributing factor in the process leading to diabetes, or a defense response against ongoing beta-cell destruction.

Somatostatin analogues were tested on a human endocrine pancreatic tumour cell line and cultured pancreatic islets. Somatostatin analogues had an effect on cAMP accumulation, chromogranin A secretion and MAP kinase activity in the cell line. Treatment of rat pancreatic islets with somatostatin analogues with selective receptor affinity was not sufficient to induce an inhibition of insulin and glucagon secretion. However, a combination of selective analogues or non-selective analogues via co-stimulation of receptors can cause inhibition of hormone production. For insulin and glucagon, combinations of sst2 + sst5 and sst1 + sst2, respectively, showed a biological effect.

In summary, knowledge of islet cell ssts expression and the effect of somatostatin analogues with high affinity to ssts may be valuable in the future attempts to influence beta-cell function in type 1 diabetes mellitus, since down-regulation of beta-cell function may promote survival of these cells during the autoimmune attack.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2006. 45 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 94
Cell biology, somatostatin, somatostatin receptors, somatostatin analogues, NOD mouse, type 1 diabetes, pancreatic islets, BON-1 cells, Cellbiologi
National Category
Cell Biology
urn:nbn:se:uu:diva-6249 (URN)91-554-6428-9 (ISBN)
Public defence
2006-02-03, B21, Biomedicinskt centrum, Husargatan 3, Uppsala, 09:15
Available from: 2006-01-13 Created: 2006-01-13Bibliographically approved

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