1986 Fiscal Year Final Research Report Summary
The role of somatostatin in pathophysiology of obesity and diabetes mellitus
| Project/Area Number |
60570529
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Kyoto University |
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Principal Investigator |
SEINO Yutaka Division of Metabolism and Clinical Nutrition, Kyoto University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (40030986)
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| Co-Investigator(Kenkyū-buntansha) |
TAMINATO Tomohiko Division of Metabolism and Clinical Nutrition, Kyoto University, Faculty of Medi, 医学部, 助手 (90107954)
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| Project Period (FY) |
1985 – 1986
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| Keywords | Somatostatin / Vagus / Cholinergic neuron / Non cholinergic neuron / Obesity |
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| Research Abstract |
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.
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