Ani Das, V; Finla, Chathu; Paulose,C S(Department of Bio Technology, April 20, 2006)
[+]
[-]
Abstract:
Sympathetic stimulation inhibits insulin secretion. a2-Adrenergic receptor is known to have a regulatory role in the sympathetic function. We
investigated the changes in the a2-adrenergic receptors in the brain stein and pancreatic islets using [3H]Yohimbine during pancreatic regeneration
in weanling rats. Brain stem and pancreatic islets of experimental rats showed a significant decrease (p<0.001) in norepinephrine (NE) content at
72 h after partial pancreatectomy. The epinephrine (EPI) content showed a significant decrease (p<0.001) in pancreatic islets while it was not
detected in brain stem at 72 h after partial pancreatectomy. Scatchard analysis of [3H]Yohimbine showed a significant decrease
(p<0.05) and Kd at 72 h after partial pancreatectomy in the brain stem. In the pancreatic islets, Scatchard analysis of [3H]Yohimbine showed a signiinfiBca'nnatx
decrease (p<0.001) in B,nax and Kd (p<0.05) at 72 h after partial pancreatectomy. The binding parameters reversed to near sham by 7 days after
pancreatectomy both in brain stein and pancreatic islets. This shows that pancreatic insulin secretion is influenced by central nervous system inputs
from the brain stem. In vitro studies with yohimbine showed that the a2-adrenergic receptors are inhibitory to islet DNA synthesis and insulin
secretion. Thus our results suggest that decreased a2-adrenergic receptors during pancreatic regeneration functionally regulate insulin secretion
and pancreatic 13-cell proliferation in weanling rats.
Eswar Shankar,P N; Santhosh,K T; Paulose,C S(Department of Biotechnology, March , 2006)
[+]
[-]
Abstract:
The stimulatory effect of dopamine through dopamine 1)2
receptor on glucose - induced insulin secretion was studied in the
pancreatic islets in nitro. I)oparnilie signifieanlly stimula(ed insulin
secretion at a concentration of 10 a N1 in the presence of
high,glucose ( 20 nii1 ). ' fhe higher concentrations of dopamine
(111 -1() 4) inhibited glucose- induced insulin secretion in the
presence of both 4 mM1 and 20 m M glucose. Stimulatory and
inhibitory effect of dopamine on glucose - induced insulin secretion
was reverted by the addition of dopamine 1)2 receptor antagonists
such as butaclamol and sulpiride . Norepinephrine (NE) at 111 4 11
concentration inhibited the dopamine uptake as well as its
stimulatory effect at 11) - 8 IN1 concentration on glucose induced
insulin secretion. Our results suggest that dopamine exerts a
differential effect on glucose -induced insulin secretion through
dopamine D2 receptor and it is essential for the regulation of
glucose-induced insulin secretion by pancreatic islets.
Renuka, T R; Remya, Robinson; Paulose,C S(Department of Biotechnology, November 2, 2005)
[+]
[-]
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.