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1. Introduction
2. Stimulus-secretion coupling
3. Ca2+ signalling and pancreatitis
4. Hyperstimulation protocol - a model for pancreatitis
5. How does hyperstimulation elicit [Ca2+]i elevation?
6. Effect of bile acids on pancreatic acinar cells
7. Effect of alcohol on Ca2+ signal generation
8. Effect of non-oxidative alcohol metabolites
9. BNPP reduces the POAEE-elicited [Ca2+]i rise
10. POA reduces cellular ATP content
11. ATP protects against toxic Ca2+ overloading
12. Action of non-oxidative alcohol metabolites
13. Acute pancreatitis: potential therapeutic targets
14. Caffeine is an IP3R antagonist
15. Coffee has a protective effect against pancreatitis
16. What caffeine can do and what it cannot do
17. Mechanisms of action of FAEEs and FAs

Topics Covered

• Normal Calcium signaling events in pancreatic acinar cells
• Hyperstimulation as a cause of sustained global elevation of the cytosolic [Calcium], Calcium-dependent vacuolization and Calcium-dependent protease activation
• Bile acids causing sustained global Calcium signals and necrosis
• Calcium-dependent necrosis evoked by non-oxidative alcohol metabolites (fatty acid ethyl esters and fatty acids) but not by alcohol or acetaldehyde
• The mechanism of action of fatty acid ethyl esters and fatty acids
• The mildly protective effect of coffee (caffeine)
• A model for the initiation of alcoholic pancreatitis

Links

Series:

• Calcium Signaling I
• Calcium Signaling II

Categories:

• Biochemistry
• Cell Biology
• Clinical Practice

Therapeutic Areas:

• Cardiovascular & Metabolic

Talk Citation

Publication History

• Published on October 1, 2007

Financial Disclosures

• Prof. Ole Petersen has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.