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Proton pump inhibitors inhibit pancreatic secretion: role of gastric and non-gastric H+/K+-ATPases

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Proton pump inhibitors inhibit pancreatic secretion : role of gastric and non-gastric H+/K+-ATPases. / Wang, Jing; Barbuskaite, Dagne; Tozzi, Marco; Giannuzzo, Andrea; Sørensen, Christiane Elisabeth; Novak, Ivana.

I: PloS one, Bind 10, Nr. 5, e0126432, 2015.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Wang, J, Barbuskaite, D, Tozzi, M, Giannuzzo, A, Sørensen, CE & Novak, I 2015, 'Proton pump inhibitors inhibit pancreatic secretion: role of gastric and non-gastric H+/K+-ATPases' PloS one, bind 10, nr. 5, e0126432. DOI: 10.1371/journal.pone.0126432

APA

Wang, J., Barbuskaite, D., Tozzi, M., Giannuzzo, A., Sørensen, C. E., & Novak, I. (2015). Proton pump inhibitors inhibit pancreatic secretion: role of gastric and non-gastric H+/K+-ATPases. PloS one, 10(5), [e0126432]. DOI: 10.1371/journal.pone.0126432

Vancouver

Wang J, Barbuskaite D, Tozzi M, Giannuzzo A, Sørensen CE, Novak I. Proton pump inhibitors inhibit pancreatic secretion: role of gastric and non-gastric H+/K+-ATPases. PloS one. 2015;10(5). e0126432. Tilgængelig fra, DOI: 10.1371/journal.pone.0126432

Author

Wang, Jing ; Barbuskaite, Dagne ; Tozzi, Marco ; Giannuzzo, Andrea ; Sørensen, Christiane Elisabeth ; Novak, Ivana. / Proton pump inhibitors inhibit pancreatic secretion : role of gastric and non-gastric H+/K+-ATPases. I: PloS one. 2015 ; Bind 10, Nr. 5.

Bibtex

@article{906e5582682443079e18b631c73cc77d,
title = "Proton pump inhibitors inhibit pancreatic secretion: role of gastric and non-gastric H+/K+-ATPases",
abstract = "The mechanism by which pancreas secretes high HCO3- has not been fully resolved. This alkaline secretion, formed in pancreatic ducts, can be achieved by transporting HCO3- from serosa to mucosa or by moving H+ in the opposite direction. The aim of the present study was to determine whether H+/K+-ATPases are expressed and functional in human pancreatic ducts and whether proton pump inhibitors (PPIs) have effect on those. Here we show that the gastric HKα1 and HKβ subunits (ATP4A; ATP4B) and non-gastric HKα2 subunits (ATP12A) of H+/K+-ATPases are expressed in human pancreatic cells. Pumps have similar localizations in duct cell monolayers (Capan-1) and human pancreas, and notably the gastric pumps are localized on the luminal membranes. In Capan-1 cells, PPIs inhibited recovery of intracellular pH from acidosis. Furthermore, in rats treated with PPIs, pancreatic secretion was inhibited but concentrations of major ions in secretion follow similar excretory curves in control and PPI treated animals. In addition to HCO3-, pancreas also secretes K+. In conclusion, this study calls for a revision of the basic model for HCO3- secretion. We propose that proton transport is driving secretion, and that in addition it may provide a protective pH buffer zone and K+ recirculation. Furthermore, it seems relevant to re-evaluate whether PPIs should be used in treatment therapies where pancreatic functions are already compromised.",
author = "Jing Wang and Dagne Barbuskaite and Marco Tozzi and Andrea Giannuzzo and S{\o}rensen, {Christiane Elisabeth} and Ivana Novak",
year = "2015",
doi = "10.1371/journal.pone.0126432",
language = "English",
volume = "10",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - Proton pump inhibitors inhibit pancreatic secretion

T2 - P L o S One

AU - Wang,Jing

AU - Barbuskaite,Dagne

AU - Tozzi,Marco

AU - Giannuzzo,Andrea

AU - Sørensen,Christiane Elisabeth

AU - Novak,Ivana

PY - 2015

Y1 - 2015

N2 - The mechanism by which pancreas secretes high HCO3- has not been fully resolved. This alkaline secretion, formed in pancreatic ducts, can be achieved by transporting HCO3- from serosa to mucosa or by moving H+ in the opposite direction. The aim of the present study was to determine whether H+/K+-ATPases are expressed and functional in human pancreatic ducts and whether proton pump inhibitors (PPIs) have effect on those. Here we show that the gastric HKα1 and HKβ subunits (ATP4A; ATP4B) and non-gastric HKα2 subunits (ATP12A) of H+/K+-ATPases are expressed in human pancreatic cells. Pumps have similar localizations in duct cell monolayers (Capan-1) and human pancreas, and notably the gastric pumps are localized on the luminal membranes. In Capan-1 cells, PPIs inhibited recovery of intracellular pH from acidosis. Furthermore, in rats treated with PPIs, pancreatic secretion was inhibited but concentrations of major ions in secretion follow similar excretory curves in control and PPI treated animals. In addition to HCO3-, pancreas also secretes K+. In conclusion, this study calls for a revision of the basic model for HCO3- secretion. We propose that proton transport is driving secretion, and that in addition it may provide a protective pH buffer zone and K+ recirculation. Furthermore, it seems relevant to re-evaluate whether PPIs should be used in treatment therapies where pancreatic functions are already compromised.

AB - The mechanism by which pancreas secretes high HCO3- has not been fully resolved. This alkaline secretion, formed in pancreatic ducts, can be achieved by transporting HCO3- from serosa to mucosa or by moving H+ in the opposite direction. The aim of the present study was to determine whether H+/K+-ATPases are expressed and functional in human pancreatic ducts and whether proton pump inhibitors (PPIs) have effect on those. Here we show that the gastric HKα1 and HKβ subunits (ATP4A; ATP4B) and non-gastric HKα2 subunits (ATP12A) of H+/K+-ATPases are expressed in human pancreatic cells. Pumps have similar localizations in duct cell monolayers (Capan-1) and human pancreas, and notably the gastric pumps are localized on the luminal membranes. In Capan-1 cells, PPIs inhibited recovery of intracellular pH from acidosis. Furthermore, in rats treated with PPIs, pancreatic secretion was inhibited but concentrations of major ions in secretion follow similar excretory curves in control and PPI treated animals. In addition to HCO3-, pancreas also secretes K+. In conclusion, this study calls for a revision of the basic model for HCO3- secretion. We propose that proton transport is driving secretion, and that in addition it may provide a protective pH buffer zone and K+ recirculation. Furthermore, it seems relevant to re-evaluate whether PPIs should be used in treatment therapies where pancreatic functions are already compromised.

U2 - 10.1371/journal.pone.0126432

DO - 10.1371/journal.pone.0126432

M3 - Journal article

VL - 10

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 5

M1 - e0126432

ER -

ID: 149040928