Modulation of insulin secretion from beta-cells by phosphoinositide-derived second-messenger molecules
Modulation of insulin secretion from beta-cells by phosphoinositide-derived second-messenger molecules. W S Zawalich Yale University School of Nursing, New Haven, Connecticut 06536. Abstract In isolated islets, the hydrolysis of membrane phosphoinositides (PI) participates in the transduction of bot...
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Published in | Diabetes (New York, N.Y.) Vol. 37; no. 2; pp. 137 - 141 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
American Diabetes Association
01.02.1988
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Online Access | Get full text |
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Summary: | Modulation of insulin secretion from beta-cells by phosphoinositide-derived second-messenger molecules.
W S Zawalich
Yale University School of Nursing, New Haven, Connecticut 06536.
Abstract
In isolated islets, the hydrolysis of membrane phosphoinositides (PI) participates in the transduction of both extracellular
and intracellular signals into an effective insulin secretory response. A wide variety of potential second-messenger molecules
are generated during the phospholipase C-mediated cleavage of these strategically situated membrane phospholipids. Several
distinct but interrelated issues are addressed in this perspective. These include 1) methodological approaches utilized to
assess PI turnover, 2) the synergistic relationship between PI-derived second messengers and cAMP, 3) the contribution of
changing PI turnover rates to the biphasic pattern of insulin output induced by 20 mM glucose, and 4) the role played by PI
turnover in the phenomenon of "memory" displayed by islets after prior stimulation with various agonists. The concept that
events unique to PI turnover contribute to beta-cell activation is well founded. Because of uncertainty regarding the exact
nature of all PI-derived messengers, however, it is not yet possible to mold the available information into a comprehensive
theory of beta-cell activation. Future studies will have to address various important unresolved issues. |
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ISSN: | 0012-1797 1939-327X 0012-1797 |
DOI: | 10.2337/diabetes.37.2.137 |