The role of somatostatin in pathophysiology of obesity and diabetes mellitus

点击翻译按钮获取中文摘要

We have found previously that somatostatin secretion is enhanced and somatostatin metabolism is delayed in obese and diabetic animals, resulting in hypersomatostatinemia which may play an important role in pathophysiology of obesity and diabetes mellitus. Since somatostatin is thought to be neuropeptide, it is important to elucidate the mechanism of neural regulation of somatostatin secretion. We have developped a new in vitro procedure of the isolated rat pancreas or stomach with vagal innervation. Electrical vagal stimulation produced an inhibition in somatostatin release. When atropine was infused, somatostatin release induced by vagal was enhanced. In the presence of hexamethonium, vagal stimulation failed to affect somatostatin secretion. Propranolol did not influence somatostatin response to vagal stimulation as phentolamine did. Simultaneous administration of propranolol and phentholamine had no effect on somatostatin response. These findings suggest that somatostatin secretion is controlled not only a cholinergic inhibitory neuron but also by a noncholinergic, e.g. peptidergic stimulatory neuron, both of which is regulated through preganglionic vagal fibers via nicotinic receptor.