Multiple effects of increases in phosphoinositide hydrolysis on islets and their relationship to changing patterns of insulin secretion.
Evidence continues to accumulate which suggests that increases in phosphoinositide hydrolysis play an integral role in beta cell insulin secretory response patterns. In the present report some of the methodological approaches utilized to monitor phosphoinositide-hydrolysis in islets are reviewed. The contribution of phosphoinositide-derived second messenger molecules to acute insulin release as well as the induction of time dependent potentiation are also discussed. Finally, the role of impaired phosphoinositide hydrolysis in the induction of time dependent suppression of insulin release is also explored. It is concluded that alterations in phosphoinositide hydrolysis contribute, at least in part, to both ordered and disordered patterns of insulin release noted under a variety of experimental conditions.
Zawalich
W
W
Yale University School of Nursing, New Haven, CT 06536-0740.
D000818:Animals; D006868:Hydrolysis; D007295:Inositol Phosphates / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism / Q000502:physiology*; D007700:Kinetics; D010716:Phosphatidylinositols / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism; D015290:Second Messenger Systems
D007295:Inositol Phosphates; D007328:Insulin; D010716:Phosphatidylinositols; D011493:Protein Kinase C