PMID: 6110594Dec 1, 1980Paper

Increased somatostatin secretion from pancreatic islets of streptozotocin-diabetic rats in response to glucose

Molecular and Cellular Endocrinology
P SchauderW Creutzfeldt

Abstract

Glucose stimulates somatostatin release from perifused pancreatic islets of diabetic rats 42-47 days after the induction of diabetes, and 48 h after withdrawal of insulin replacement therapy. The glucose effect is augmented by theophylline or glucagon. Basal somatostatin release and glucose-induced secretion are significantly higher in diabetic islets than in controls. It is suggested that glucose promotes somatostatin release by directly interacting with islet D cells but not via indirect pathways. Glucose-induced stimulation appears to be modulated by a D-cell adenylate cyclase/phosphodiesterase system. Reasons responsible for increased somatostatin secretion by diabetic islets include reduction in B-cell mass, suggesting that B cells may normally suppress the secretory activity of D cells.

References

Oct 1, 1977·Analytical Biochemistry·U PantenA Hasselblatt
Apr 1, 1976·Proceedings of the National Academy of Sciences of the United States of America·L OrciR H Unger
Jan 1, 1978·Annual Review of Physiology·R H UngerL Orci
May 1, 1977·Proceedings of the National Academy of Sciences of the United States of America·G S PattonR H Unger
Nov 17, 1975·Biochemical and Biophysical Research Communications·P SchauderH Frerichs

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Citations

Nov 1, 1983·The Journal of Surgical Research·R H Bell, R J Hye
Jun 1, 1984·The American Journal of Physiology·V Grill, S Efendić

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