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[Purinergic receptors and insulin secretion]
Journal De Pharmacologie
|October 1, 1983
Summary
Adenosine triphosphate (ATP) stimulates insulin secretion in a dose-dependent manner, suggesting a role for purinergic receptors on beta cells. This effect is specific to ATP and ADP, highlighting a structure-activity relationship for insulin release.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- Adenosine triphosphate (ATP) is known to stimulate insulin secretion.
- Understanding the precise mechanisms and receptor interactions involved is crucial for metabolic research.
Purpose of the Study:
- To investigate the dose-dependent and structural requirements of ATP's effect on insulin secretion.
- To identify the specific purinergic receptor subtype involved in ATP-mediated insulin release.
Main Methods:
- Kinetic study using an isolated perfused rat pancreas model.
- Evaluation of various natural nucleotides and structural analogues of ATP/ADP.
- Assessment of antagonist effects using specific blocking agents.
Main Results:
- ATP demonstrated a biphasic, dose-dependent insulin secretory response (10^-6 to 10^-4 M).
- A purine base and 2-3 phosphate groups were essential for insulin secretion.
- Theophylline and adrenergic/cholinergic blockers did not inhibit ATP's action, but 2,2' pyridylisatogen selectively antagonized it.
Conclusions:
- Results strongly suggest the involvement of a purinergic receptor, likely a P2 type, on pancreatic beta cells.
- The structure-activity relationship indicates specific molecular features of ATP/ADP are necessary for insulin stimulation.
- ATP and ADP act as key signaling molecules in insulin secretion regulation via specific receptor interactions.