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A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
Published on: July 16, 2016
P2 receptor agonists stimulate insulin release from human pancreatic islets
J Fernandez-Alvarez1, D Hillaire-Buys, M M Loubatières-Mariani
1Endocrinology and Diabetes Unit, Hospital Clinic i Universitari, Barcelona, Spain.
Pancreas
|January 4, 2001
Summary
P2 receptor agonists, such as alpha,beta-methylene ATP, stimulate insulin secretion in human pancreatic islets. This effect is glucose-dependent, particularly for P2Y receptor activation, offering new insights into glucose regulation.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- P2 receptors for adenosine 5'-triphosphate (ATP) and adenosine 5'-diphosphate (ADP) are present in mammalian pancreatic beta cells.
- Previous studies lacked evidence for P2 receptor agonist-induced insulin secretion in humans.
Purpose of the Study:
- To investigate the potential of P2 receptor agonists to stimulate insulin release in human pancreatic islets.
- To determine the glucose dependency of P2 receptor agonist-mediated insulin secretion in humans.
Main Methods:
- Human pancreatic islets from organ donors were utilized.
- Experiments involved varying glucose concentrations (3.0 and 8.3 mmol/L).
- Insulin release was quantified using radioimmunoassay.
- The effects of alpha,beta-methylene ATP and ADPbetaS were assessed.
Main Results:
- At a slightly stimulating glucose concentration (8.3 mmol/L), both alpha,beta-methylene ATP and ADPbetaS significantly amplified insulin secretion (threefold increase).
- At a non-stimulating glucose concentration (3.0 mmol/L), only alpha,beta-methylene ATP induced a significant insulin release (1.4-fold increase), while ADPbetaS was ineffective.
- The results indicate that P2 receptor agonists can stimulate insulin release in humans.
Conclusions:
- P2 receptor agonists are effective in stimulating insulin release from human pancreatic islets.
- The insulin-releasing effect of the P2Y receptor agonist is significantly dependent on glucose concentration.
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