Enhanced beta-adrenergic receptors in the brain and pancreas during pancreatic regeneration in weanling rats.

Adrenergic stimulation has an important role in the pancreatic beta-cell proliferation and insulin secretion. In the present study, we have investigated how sympathetic system regulates the pancreatic regeneration by analyzing Epinephrine (EPI), Norepinephrine (NE) and beta-adrenergic receptor changes in the brain as well as in the pancreas. EPI and NE showed a significant decrease in the brain regions, pancreas and plasma at 72 hrs after partial pancreatectomy. We observed an increase in the circulating insulin levels at 72 hrs. Scatchard analysis using [(3)H] propranolol showed a significant increase in the number of both the low affinity and high affinity beta-adrenergic receptors in cerebral cortex and hypothalamus of partially pancreatectomised rats during peak DNA synthesis. The affinity of the receptors decreased significantly in the low and high affinity receptors of cerebral cortex and the high affinity hypothalamic receptors. In the brain stem, low affinity receptors were increased significantly during regeneration whereas there was no change in the high affinity receptors. The pancreatic beta-adrenergic receptors were also up regulated at 72 hrs after partial pancreatectomy. In vitro studies showed that beta-adrenergic receptors are positive regulators of islet cell proliferation and insulin secretion. Thus our results suggest that the beta-adrenergic receptors are functionally enhanced during pancreatic regeneration, which in turn increases pancreatic beta-cell proliferation and insulin secretion in weanling rats.