dc.contributor.author |
Renuka, T R |
|
dc.contributor.author |
Remya, Robinson |
|
dc.contributor.author |
Paulose,C S |
|
dc.date.accessioned |
2008-07-30T11:25:50Z |
|
dc.date.available |
2008-07-30T11:25:50Z |
|
dc.date.issued |
2005-11-02 |
|
dc.identifier.uri |
http://dyuthi.cusat.ac.in/purl/540 |
|
dc.description.abstract |
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. |
en_US |
dc.language.iso |
en |
en_US |
dc.publisher |
Department of Biotechnology |
en_US |
dc.subject |
Muscarinic M1 and M3 receptors |
en_US |
dc.subject |
Insulin secretion |
en_US |
dc.subject |
Carbachol |
en_US |
dc.subject |
Atropine |
en_US |
dc.subject |
Pancreatic islets |
en_US |
dc.title |
Increased Insulin Secretion by Muscarinic M1 and M3 Receptor Function from Rat Pancreatic Islets in vitro |
en_US |
dc.type |
Working Paper |
en_US |