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Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
Published on: May 10, 2018
Serotonin receptor 2C and insulin secretion
Qiang Zhang1, Yunxia Zhu, Wenbo Zhou
1State Key Laboratory of Reproductive Medicine and Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Plos One
|January 26, 2013
Summary
Increased serotonin 2C receptor (5-HT(2C)R) expression in pancreatic cells may impair insulin secretion in type 2 diabetes. Blocking this receptor enhances insulin release, offering potential new treatments for T2DM.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Molecular Biology
Background:
- Type 2 diabetes mellitus (T2DM) involves impaired insulin secretion and sensitivity.
- High serotonin (5-hydroxytryptamine; 5-HT) levels are observed in T2DM patients.
- The role of 5-HT in T2DM-related insulin secretion is not fully understood.
Purpose of the Study:
- Investigate 5-HT receptor 2C (5-HT(2C)R) expression in diabetic mouse pancreatic islets.
- Determine the role of 5-HT(2C)R signaling in pancreatic beta-cell insulin secretion.
Main Methods:
- Examined 5-HT(2C)R expression in pancreatic islets of db/db mice (diabetic) and control mice.
- Utilized 5-HT(2C)R antagonist (SB242084) and agonist (mCPP) on isolated islets and Min-6 cells.
- Employed RNA interference to target 5-HT(2C)R in Min-6 cells.
- Treated Min-6 cells with palmitic acid to mimic diabetic conditions.
Main Results:
- 5-HT(2C)R expression was significantly elevated in pancreatic islets of db/db mice.
- 5-HT(2C)R antagonist SB242084 dose-dependently increased insulin secretion in db/db islets, but not control islets.
- 5-HT(2C)R agonist mCPP inhibited insulin secretion in Min-6 cells and islets, an effect reversed by SB242084 or 5-HT(2C)R knockdown.
- Palmitic acid increased 5-HT(2C)R expression in Min-6 cells, and SB242084 reversed palmitic acid-induced inhibition of insulin secretion.
Conclusions:
- Elevated 5-HT(2C)R expression in pancreatic beta-cells appears to inhibit insulin secretion in T2DM.
- Targeting 5-HT(2C)R signaling presents a potential therapeutic strategy for T2DM.
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