Increased somatostatin secretion from pancreatic islets of streptozotocin-diabetic rats in response to glucose.
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.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005934:Glucagon / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D013004:Somatostatin / Q000378:metabolism*; D013806:Theophylline / Q000494:pharmacology
D013004:Somatostatin; D005934:Glucagon; D013806:Theophylline; D005947:Glucose