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Peripherally administered serotonin induces hyperglucagonemia in mice
J Yamada1, Y Sugimoto, I Kimura
1Department of Pharmacology, Kobe Women's College of Pharmacy, Japan.
Life Sciences
|January 1, 1993
Summary
Peripherally administered serotonin (5-HT) significantly increased plasma glucagon in mice. This effect was blocked by 5-HT2 receptor antagonists, suggesting these receptors regulate glucagon release.
Area of Science:
- Endocrinology
- Neuroscience
- Pharmacology
Background:
- Serotonin (5-HT) is a neurotransmitter with diverse physiological roles.
- The role of peripheral serotonin in regulating glucagon secretion is not fully understood.
Purpose of the Study:
- To investigate the effect of peripheral serotonin on plasma glucagon levels in mice.
- To identify the specific serotonin receptor subtypes involved in mediating these effects.
Main Methods:
- Mice were administered serotonin (5-HT) peripherally.
- Plasma glucagon levels were measured.
- The effects of specific serotonin receptor antagonists (methysergide, ketanserin, ritanserin, ICS 205-930, MDL 72222) were assessed.
Main Results:
- Peripherally administered serotonin caused a significant increase in plasma glucagon.
- This hyperglucagonemic effect was completely blocked by antagonists with high affinity for 5-HT2 receptors.
- 5-HT3 receptor antagonists did not affect the serotonin-induced increase in glucagon.
Conclusions:
- Activation of peripheral 5-HT2 receptors stimulates an increase in plasma glucagon levels.
- These findings suggest a role for peripheral 5-HT2 receptors in the regulation of glucagon release.