Increased Insulin Secretion by Muscarinic M1 and M3 Receptor Function from Rat Pancreatic Islets in vitro

Parasympathetic system plays an important role in insulin secretion from the pancreas. Cholinergic effect on pancreatic beta cells exerts primarily through muscarinic receptors. In the present study we investigated the specific role of muscarinic M1 and M3 receptors in glucose induced insulin secretion from rat pancreatic islets in vitro. The involvement of muscarinic receptors was studied using the antagonist atropine. The role of muscarinic MI and M3 receptor subtypes was studied using subtype specific antagonists. Acetylcholine agonist, carbachol, stimulated glucose induced insulin secretion at low concentrations (10-8-10-5 M) with a maximum stimulation at 10-7 M concentration. Carbachol-stimulated insulin secretion was inhibited by atropine confirming the role of muscarinic receptors in cholinergic induced insulin secretion. Both M1 and M3 receptor antagonists blocked insulin secretion induced by carbachol. The results show that M3 receptors are functionally more prominent at 20 mM glucose concentration when compared to MI receptors. Our studies suggest that muscarinic M1 and M3 receptors function differentially regulate glucose induced insulin secretion, which has clinical significance in glucose homeostasis.

MUSCARINIC M1 AND M3 RECEPTOR GENE EXPRESSION DURING PANCREATIC REGENERATION AND INSULIN SECRETION IN RATS

The present work is an attempt to understand the role of acetylcholine muscarinic M1 and M3 receptors during pancreatic regeneration and insulin secretion. The work focuses on the changes in the muscarinic M1 and M3 receptors in brain and pancreas during pancreatic regeneration. The effect of these receptor subtypes on insulin secretion and pancreatic P-cell proliferation were studied in vitro using rat primary pancreatic islet culture. Muscarinic Ml and M3 receptor kinetics and gene expression studies during pancreatic regeneration and insulin secretion will help to elucidate the role of acetylcholine functional regulation of pancreatic u-cell proliferation and insulin secretion.The cholinergic system through muscarinic M1 and M3 receptors play an important role in the regulation of pancreatic (3-cell proliferation and insulin secretion . Cholinergic activity as indicated by acetylcholine esterase, a marker for cholinergic system, decreased in the brain regions - hypothalamus, brain stem, corpus striatum, cerebral cortex and cerebellum during pancreatic regeneration. Pancreatic muscarinic M1 and M3 receptor activity increased during proliferation indicating that both receptors are stimulatory to (3-cell division. Acetylcholine dose dependently increase EGF induced DNA synthesis in pancreatic islets in vitro, which is inhibited by muscarinic antagonist atropine confirming the role of muscarinic receptors. Muscarinic M1 and M3 receptor antagonists also block acetycholine induced DNA synthesis suggesting the importance of these receptors in regeneration. Acetylcholine also stimulated glucose induced insulin secretion in vitro which is inhibited by muscarinic M1 and M3 receptor antagonists. The muscarinic receptors activity and their functional balance in the brain and pancreas exert a profound influence in the insulin secretion and also regeneration of pancreas

Comparative efficacy of MS-222 and benzocaine as anaesthetics under simulated transport conditions of a tropical ornamental fish Puntius filamentosus(Valenciennes)

There is a growing commercial interest in the ¢sh, Puntius ¢lamentosus, in the ornamental ¢sh trade in India and elsewhere.The trade is, however, hampered by severe mortalities during transport of the ¢sh owing to insu⁄cient data available on the use of anaesthetics. To resolve this problem, we evaluated the e⁄cacy of two anaesthetics, MS-222 and benzocaine, in sedating P. ¢lamentosus in simulated transportation experiments and used stress response parameters such as cortisol and blood glucose levels to perform assessments. We observed that MS-222 at 40 mg L 1 and benzocaine at 20mg L 1 were su⁄- cient to induce sedation for 48 h. Above these concentrations, both the anaesthetics adversely a¡ected the ¢sh and resulted inmortalities. Both anaesthetics signi¢cantly lowered the blood cortisol and glucose levels compared with the unsedated controls. Importantly, the anaesthetics treatment signi¢cantly lowered the post-transport mortality in the ¢sh. The results of the study show that MS-222 and benzocaine could be used as sedatives to alleviate transport- related stress in P. ¢lamentosus to improve their post-transport survival and hence reduce economic loss.