uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Somatostatin Receptor Subtypes in Human Type 2 Diabetic Islets
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemical endocrinology.
2010 (English)In: Pancreas, ISSN 0885-3177, E-ISSN 1536-4828, Vol. 39, no 6, p. 836-842Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2010. Vol. 39, no 6, p. 836-842
Keywords [en]
somatostatin receptors, pancreas, human, type 2 diabetes, immunohistochemistry
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-124341DOI: 10.1097/MPA.0b013e3181cf1878ISI: 000280190900014PubMedID: 20182388OAI: oai:DiVA.org:uu-124341DiVA, id: diva2:317363
Available from: 2010-05-03 Created: 2010-05-03 Last updated: 2017-12-12Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMed

Authority records BETA

Grimelius, LarsWestermark, PerStridsberg, Mats

Search in DiVA

By author/editor
Grimelius, LarsWestermark, PerStridsberg, Mats
By organisation
Department of Genetics and PathologyBiochemical endocrinology
In the same journal
Pancreas
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 3846 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf