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Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
Published on: May 11, 2015
Somatostatin receptor subtypes in human type 2 diabetic islets
Guida M Portela-Gomes1, Lars Grimelius, Per Westermark
1Department of Gastroenterology, Lisbon University, Lisbon, Portugal. portela_gomes@yahoo.com
In type 2 diabetes, somatostatin receptor (sst) patterns change in pancreatic islet cells, particularly in somatostatin, glucagon, and pancreatic polypeptide cells. These alterations may impact islet function and require further investigation.
Area of Science:
- Endocrinology
- Cell Biology
- Metabolic Diseases
Background:
- Somatostatin receptors (sst1-sst5) regulate hormone release.
- The specific role of somatostatin in islet physiology, especially in diabetes, remains incompletely understood.
- Previous studies have characterized sst1-sst5 expression in normal human pancreas.
Purpose of the Study:
- To investigate the expression patterns of somatostatin receptors (sst1-sst5) in human pancreatic islets from individuals with type 2 diabetes mellitus.
- To compare these expression patterns with those in non-diabetic controls.
Main Methods:
- Utilized pancreatic autopsy specimens from type 2 diabetes patients and matched controls.
- Employed double immunostaining techniques to identify sst1-sst5 expression in major islet cell types.
Main Results:
- Type 2 diabetic islets showed distinct sst patterns compared to controls.
- Notable differences included the absence of sst1 and sst4 in glucagon cells and sst1-3 and 4 in somatostatin cells.
- Pancreatic polypeptide cells exhibited a reversed sst staining pattern in diabetic individuals.
- Minor alterations were observed in insulin cells.
Conclusions:
- Significant differences in somatostatin receptor (sst) expression patterns exist between type 2 diabetic and control human pancreatic islets.
- These changes were most prominent in somatostatin, pancreatic polypeptide, and glucagon cells.
- The precise cause of these sst pattern alterations (direct diabetes effect vs. secondary metabolic changes) requires further research.
- This study provides a foundation for future functional investigations into the role of sst1-sst5 in type 2 diabetes.
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