These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Somatostatin receptor subtypes in human type 2 diabetic islets.
    Author: Portela-Gomes GM, Grimelius L, Westermark P, Stridsberg M.
    Journal: Pancreas; 2010 Aug; 39(6):836-42. PubMed ID: 20182388.
    Abstract:
    OBJECTIVES: Somatostatin inhibits hormone release through 5 G protein-coupled somatostatin receptors (sst1-sst5). However, the role of somatostatin in islet physiology is not fully known. The immunoreactivity to sst1 to sst5 in normal human endocrine pancreas has been described. The present study reports the expression of sst1 to sst5 in human pancreatic islets with type 2 diabetes mellitus. METHODS: Pancreatic autopsy specimens from individuals with type 2 diabetes mellitus and matched controls were double immunostained to demonstrate sst1 to sst5 in the major islet cell types. RESULTS: Most apparent differences in type 2 diabetic islets were the lack of sst1 and sst4 in glucagon cells and sst1-3 and 4 in somatostatin cells, whereas minor changes were demonstrated in insulin cells. The pancreatic polypeptide cells showed a reversed staining pattern in diabetic islets compared with the controls. CONCLUSIONS: In type 2 diabetes mellitus, the sst pattern differed from that of the controls in somatostatin, pancreatic polypeptide, and glucagon cells, to a minor extent in insulin cells. It is unclear whether the changes in sst patterns are primarily due to the diabetes or secondary to metabolic disturbances. However, this study may be the basis for further functional studies to evaluate the role of sst1 to sst5 in the diabetic state.
    [Abstract] [Full Text] [Related] [New Search]