[Frontiers in Bioscience 2, d160-172, March 15, 1997]
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SIGNAL TRANSDUCTION IN PANCREATIC ß-CELLS: REGULATION OF INSULIN SECRETION BY INFORMATION FLOW IN THE PHOSPHOLIPASE C/PROTEIN KINASE C PATHWAY

Walter S. Zawalich, Marc Bonnet-Eymard, and Kathleen C. Zawalich

Yale University School of Nursing, 100 Church Street South, New Haven, CT 06536-0740 USA

Received 2/24/97; Accepted 2/27/97; On-line 3/15/97

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Multiple effects of glucose on the pancreatic ß-cell
3.1 Acute regulation of insulin release
3.2 Fail-safe regulation of insulin secretion and time-dependent potentiation
3.3 Time-dependent suppression of insulin release
4. Glucose-induced insulin secretion: role of phospholipase C activation
4.1 Effects of glucose on PLC-mediated phosphoinositide (PI) hydrolysis
4.2 PLC isozymes in islets and their activation
5. Glucose-induced insulin secretion: role of protein kinase C activation
5.1 Protein kinase C activation in freshly studied rat islets
5.2 Protein kinase C activation and glucose-induced insulin secretion from cultured islets
5.3 Insulin secretion from PKC-depleted islets
6. Species differences in glucose-induced insulin secretion
6.1 Glucose-induced insulin release from mouse islets
6.2 PLC activation in mouse islets
6.3 Time-dependent potentiation in mouse islets
6.4 Glucose fails to induce time-dependent suppression in mouse islets
7. The beta cell, obesity and NIDDM
8. Summary and Perspectives
9. References
10. Entire manuscript

Key words: Phospholipase C, protein kinase C, insulin secretion, islets, ß-cell, phosphoinositide hydrolysis, time-dependent potentiation, time-dependent suppression

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