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Printable Handouts
Navigable Slide Index
- Introduction
- Stimulus-secretion coupling
- Ca2+ signalling and pancreatitis
- Hyperstimulation protocol - a model for pancreatitis
- How does hyperstimulation elicit [Ca2+]i elevation?
- Effect of bile acids on pancreatic acinar cells
- Effect of alcohol on Ca2+ signal generation
- Effect of non-oxidative alcohol metabolites
- BNPP reduces the POAEE-elicited [Ca2+]i rise
- POA reduces cellular ATP content
- ATP protects against toxic Ca2+ overloading
- Action of non-oxidative alcohol metabolites
- Acute pancreatitis: potential therapeutic targets
- Caffeine is an IP3R antagonist
- Coffee has a protective effect against pancreatitis
- What caffeine can do and what it cannot do
- 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
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Talk Citation
Petersen, O. (2007, October 1). Pancreatitis and calcium signaling [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 7, 2024, from https://doi.org/10.69645/NCYC1942.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Ole Petersen has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.