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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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