Decreased a2-adrenergic receptor in the brain stem and pancreatic islets during pancreatic regeneration in weanling rats

Content Provider	CUSAT-Thesis
Author	Ani Das, V. Finla, Chathu Paulose, C. S.
Abstract	Sympathetic stimulation inhibits insulin secretion. a2-Adrenergic receptor is known to have a regulatory role in the sympathetic function. Weinvestigated the changes in the a2-adrenergic receptors in the brain stein and pancreatic islets using [3H]Yohimbine during pancreatic regenerationin weanling rats. Brain stem and pancreatic islets of experimental rats showed a significant decrease (p<0.001) in norepinephrine (NE) content at72 h after partial pancreatectomy. The epinephrine (EPI) content showed a significant decrease (p<0.001) in pancreatic islets while it was notdetected 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'nnatxdecrease (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 afterpancreatectomy both in brain stein and pancreatic islets. This shows that pancreatic insulin secretion is influenced by central nervous system inputsfrom the brain stem. In vitro studies with yohimbine showed that the a2-adrenergic receptors are inhibitory to islet DNA synthesis and insulinsecretion. Thus our results suggest that decreased a2-adrenergic receptors during pancreatic regeneration functionally regulate insulin secretionand pancreatic 13-cell proliferation in weanling rats.
File Format	PDF
Language	English
Publisher	Department of Bio Technology
Access Restriction	Open
Subject Keyword	a2-Adrenergic receptors Pancreatectomy Brain stem Pancreatic islets Insulin secretion
Content Type	Text
Resource Type	Article