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Function and expression of melatonin receptors on human pancreatic islets
Reshma D Ramracheya1, Dany S Muller, Paul E Squires
1Beta Cell Development & Function Group, School of Biomedical & Health Sciences, King's College London, London, UK.
Journal of Pineal Research
|January 16, 2008
Summary
Melatonin stimulates human islet cells, increasing glucagon and insulin secretion, unlike its inhibitory effect in rodents. This highlights species-specific actions of melatonin on pancreatic islets.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Melatonin inhibits insulin secretion in rodent beta-cells via MT1/MT2 receptors.
- The role of melatonin in human pancreatic islets remains unclear.
Purpose of the Study:
- Investigate melatonin receptor expression in human islets.
- Determine the effects of melatonin on human islet cell function, including calcium levels and hormone secretion.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) for receptor mRNA expression.
- Single-cell microfluorimetry for intracellular calcium ([Ca2+]i) analysis.
- Radioimmunoassay for islet hormone secretion quantification.
Main Results:
- Human islets express MT1 and MT2 melatonin receptor mRNAs; MT1 is found in alpha-cells, not beta-cells.
- Melatonin stimulates intracellular calcium and glucagon secretion from human islets.
- Melatonin indirectly stimulates insulin secretion in human islets, likely via glucagon's paracrine action.
Conclusions:
- Melatonin directly stimulates human islet alpha-cells.
- Melatonin-induced insulin secretion in humans is a secondary effect of glucagon release.
- Melatonin exhibits species-specific effects: inhibitory in rodent beta-cells, stimulatory in human islets.
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