Author:
Efendić Suad,Enzmann Franz,Gutniak Mark,Nylén Anita,Zoltobrocki Manfred
Abstract
Abstract.
HB 699 (100 μg/ml), almost identical with the left residue of the sulphonylurea glibenclamide, enhanced basal insulin and somatostatin release from the perfused rat pancreas. The compound also augmented both the early and the late insulin release stimulated by 6.7 mm glucose, while with 16.7 and 33.3 mm glucose only late insulin release was increased. Furthermore, HB699 enhanced both phases of glucose induced somatostatin release irrespective of whether 6.7, 16.7 or 33.3 mM glucose were used. As for glucagon release, HB 699 suppressed basal and arginine stimulated glucagon secretion.
The present findings imply that the sulphonylurea moiety of glibenclamide is not a prerequisite for its stimulatory action on insulin and somatostatin release. It is suggested that the enhanced somatostatin release mediates the inhibitory effect of the compound on glucagon release.
Subject
Endocrinology,General Medicine,Endocrinology, Diabetes and Metabolism
Cited by
8 articles.
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