A STUDY ON THE MECHANISM OF TOLBUTAMIDE-INDUCED INSULIN SECRETION ESPECIALLY ON THE C'-AMP

• Published in: Journal of The Showa Medical Association Vol. 37; no. 3; pp. 263 - 272
• Main Author: Tsuji, Masatomi
• Format: Journal Article
• Language: English; Japanese
• Published: The Showa University Society 28.06.1977
• ISSN: 0037-4342; 2185-0976
• DOI: 10.14930/jsma1939.37.263

Studies were performed to investigate the influence of tolbutamide on the cyclic AMP system of the islets in the normal subjects. The conclusion were as follows; 1) In the insulin response to the combined stimulation of tolbutamide and glucagon, which stimulates adenylcyclase, a synergistic effect was observed. 2) The insulin response to glucagon was markedly enhanced by tolbutamide. 3) Isoproterenol, which stimulates adenylcyclase, enhanced tolbutamide-induced insulin secretion 4) Tolbutamide-induced insulin secretion was not enhanced by aminophylline which inhibits phosphodiesterase, but glucagon-induced insulin secretion was enchanced. 5) From the results as above, it seems that tolbutamide inhibits phosphodiesterase in the B-cell of islets. 6) In each experiments, the increase of C-peptide showed a close correlation with that of insulin, and C-peptide was considered significantly to reflect the insulin secretion. 7) Peak levels of C-peptide occurred later than those of insulin and C-peptide decreased slowly to basal levels. The molar concentration of C-peptide were greater than insulin. Molar ratio (CPR : IRI) at peak levels was from 1.3 to 3.13.