The effects of acetylcholine signaling in the human pancreatic islet

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 834-867-Islet Biology
Bench to Bedside
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-855
Judith T. Molina*1, Alberto F Fachado1, Per-Olof Berggren2 and Alejandro Caicedo1
1University of Miami, Miami, FL, 2The Rolf Luft Ctr for Diab Rsr, Stockholm, Sweden
The effects of acetylcholine signaling in the human pancreatic islet

Judith Molina, Alberto Fachado, Per-Olof Berggren, and Alejandro Caicedo

Acetylcholine is a neurotransmitter that is crucial for pancreatic beta cell function and survival.  Less is known about how acetylcholine affects other endocrine cells within the pancreatic islet.  Given that acetylcholine is released from alpha cells in the human islet, we hypothesized that cholinergic paracrine signaling affects the release of other hormones and paracrine signals within the islet.  We investigated the expression of muscarinic receptors in human islet endocrine cells and found that beta cells express M3 and M5 receptors, alpha cells M4 receptors, and delta cells M1 receptors.  Activation of these receptors increased insulin and somatostatin secretion from beta and delta cells, respectively.  Activation of M4 receptors in alpha cells inhibited secretion of acetylcholine, indicating that acetylcholine regulates its own secretion via a negative feedback loop.  Our results indicate that acetylcholine activates a different set of muscarinic receptors in each endocrine cell type, thus achieving cell-specific effects in the human islet.  This allows for selective targeting in the context of therapeutic intervention in diabetes.

Nothing to Disclose: JTM, AFF, POB, AC

*Please take note of The Endocrine Society's News Embargo Policy at