Review of Literature REVIEW OF THE LITERATURE

The role of central nervous system in the regulation of glucose homeostasis has been recognized for more than a century. Research in this regard till now strongly supported a close relation between catecholamines and glucose homeostasis. Recent studies done by many authors reveals several interesting aspects on regulation of pancreatic secretion by CNS. Ho et al., (1995) demonstrated that reduction in acetylcholine (ACh) and norepinephrine (NE) potentiating effects, decreases glucose sensitivity of islet J3 and a cells in streptozotocin diabetic model. In another study by Hiyoshi et al., (1995) by intracerebroventricular (i.c.v.) administration of neostigmine, caused an increase in plasma levels of catecholamines and glucose but not insulin. When atropine was co-administered with phentolamine, the phentolamine induced increase in insulin secretion, was inhibited. But neither phentolamine nor atropine affected plasma levels of catecholamine. At the same time.o-jadrenoceptor antagonists Yohimbine and ldazoxan reversed adrenaline induced inhibition of insulin secretion and thus glucose levels (Hiyoshi et al., 1995). The results suggest that inhibition of insulin release induced by adrenaline was reversed by antagonism of a-2-adrenoceptors. lhe pancreatic function has been studied extensively in relation to CNS neuronal regulation by several others also. The enteropancreatic sympathetic nerve when analysed for its regulatory action through cholinergic and serotonergic neurons suggested that serotonergic enteropancreatic innervation inhibits pancreatic secretion via presynaptic receptors on cholinergic nerves (Kirchgessner et al., 1995). The peripheral system adrenergic receptors and nerves involved in pancreatic glucagon and insulin secretion in rabbits revealed that J3-adrenergic 4 receptor mechanism is an important component of adrenergic modulation of pancreatic glucagon secretion in conscious rabbits (Odo.., 1995). The plasma insulin concentrations were suppressed by a-adrenergic stimulation more than 0. and J3-adrenergic stimulation. The periPheral adrenergic receptor and regulation of glucose, insulin and amylin when analyzed using selective 0.-2 adrenoreceptor agonist UK 14.304 produced a dose-dependent reduction in the normal rats in their content. It is suggested that insulin and amylin are both under inhibitory control via