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Am J Physiol Gastrointest Liver Physiol (April 2, 2004). doi:10.1152/ajpgi.00035.2004
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Submitted on January 22, 2004
Accepted on March 26, 2004

Acidic Duodenal pH Alters Gene Expression in the Cystic Fibrosis Mouse Pancreas

Simran Kaur1, Oxana Norkina1, Donna Ziemer1, Linda C. Samuelson2, and Robert C. De Lisle1*

1 Department of Anatomy and Cell Biology, University of Kansas School of Medicine, Kansas City, KS, USA
2 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA

* To whom correspondence should be addressed. E-mail: rdelisle{at}kumc.edu.

The duodenum is abnormally acidic in cystic fibrosis (CF) due to decreased bicarbonate ion secretion which is dependent on the CF gene product CFTR (cystic fibrosis conductance transmembrane regulator). In the CFTR null mouse the acidic duodenum results in increased signaling from the intestine to the exocrine pancreas in an attempt to stimulate pancreatic bicarbonate ion secretion. Excess stimulation is proposed to add to the stress/inflammation of the pancreas in CF. DNA microarray analysis of the CF mouse revealed altered pancreatic gene expression characteristic of stress/inflammation. When the duodenal pH was corrected genetically (crossing CFTR null with gastrin null mice) or pharmacologically (use of the proton pump inhibitor omeprazole), expression levels of genes measured by quantitative RT-PCR were significantly normalized. It is concluded that the acidic duodenal pH in CF contributes to the stress on the exocrine pancreas and that normalizing duodenal pH reduces this stress.




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