Restoring effects of refeeding and dibutyril cyclic AMP on the increased glucagon secretion of rat pancreatic islets during starvation.
The glucagon release in the presence of glucose and the interaction of dibutyril cyclic AMP was studied in isolated pancreatic islets from fed and 96 h-fasted rats incubated for 30 min. In both states the increase of glucose concentration produced a similar inhibition of glucagon release and stimulation of cyclic AMP content. Higher glucagon secretion and lower cyclic AMP contents were observed in islets from fasted than in those from fed animals at both 2.75 and 16.7 mM glucose. Islets from rats starved for 96 h and refed for 48 h with normal diet or oral 20% glucose showed glucagon release patterns similar to those of controls. Addition of 2 mM dibutyril cyclic AMP to the incubation medium inhibited the fasting-induced increase of glucagon secretion at both glucose levels. These results show an inverse correlation between glucagon secretion and islet cyclic AMP content. However, the sensitivity of the islet to glucose-induced inhibition of glucagon secretion appears to be independent of the islet cyclic AMP levels.
D000818:Animals; D003994:Bucladesine / Q000032:analysis / Q000494:pharmacology*; D005215:Fasting; D005934:Glucagon / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D007515:Islets of Langerhans / Q000201:enzymology / Q000502:physiology*; D051381:Rats; D013268:Stimulation, Chemical; D013997:Time Factors
D003994:Bucladesine; D005934:Glucagon; D005947:Glucose