Abstract | BACKGROUND & AIMS: METHODS: We measured ΔΨm in mouse pancreatic acinar cells incubated with ethanol alone and in combination with physiologic and pathologic concentrations of cholecystokinin-8 (CCK). To examine the role of MPTP, we used ex vivo and in vivo models of pancreatitis, induced in wild-type and CypD(-/-) mice by a combination of ethanol and CCK. RESULTS: CONCLUSIONS: Oxidative metabolism of ethanol sensitizes pancreatic mitochondria to activate MPTP, leading to mitochondrial failure; this makes the pancreas susceptible to necrotizing pancreatitis.
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Authors | Natalia Shalbueva, Olga A Mareninova, Andreas Gerloff, Jingzhen Yuan, Richard T Waldron, Stephen J Pandol, Anna S Gukovskaya |
Journal | Gastroenterology
(Gastroenterology)
Vol. 144
Issue 2
Pg. 437-446.e6
(Feb 2013)
ISSN: 1528-0012 [Electronic] United States |
PMID | 23103769
(Publication Type: Comparative Study, Journal Article)
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Copyright | Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved. |
Chemical References |
- Mitochondrial Membrane Transport Proteins
- Mitochondrial Permeability Transition Pore
- Ethanol
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Topics |
- Acinar Cells
(drug effects, metabolism, pathology)
- Animals
- Disease Models, Animal
- Ethanol
(pharmacokinetics, toxicity)
- Membrane Potential, Mitochondrial
(drug effects)
- Mice
- Mitochondria
(drug effects, metabolism, pathology)
- Mitochondrial Membrane Transport Proteins
(metabolism)
- Mitochondrial Permeability Transition Pore
- Oxidative Stress
- Pancreas
(drug effects, metabolism, pathology)
- Pancreatitis, Acute Necrotizing
(etiology, metabolism, pathology)
- Pancreatitis, Alcoholic
(complications, metabolism, pathology)
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