|
|
||||||||
1 Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas 66160; and 2 Departments of Pediatrics and Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106
The exocrine pancreas of the cystic fibrosis (CF) mouse (cftrm1UNC) is only mildly affected compared with the human disease, providing a useful model to study alterations in exocrine function. The CF mouse pancreas has ~50% of normal amylase levels and ~200% normal Muclin levels, the major sulfated glycoprotein of the pancreas. Protein biosynthetic rates and mRNA levels for amylase were not altered in CF compared with normal mice, and increases in Muclin biosynthesis and mRNA paralleled the increased protein content. Stimulated pancreatic amylase secretion in vitro and in vivo tended to be increased in CF mice but was not statistically significant compared with normal mice. We show for the first time that the CF mouse duodenum is abnormally acidic (normal intestinal pH = 6.47 ± 0.05; CF intestinal pH = 6.15 ± 0.07) and hypothesize that this may result in increased signaling to the exocrine pancreas. There were significant increases in CF intestinal mRNA levels for secretin (310% of normal, P < 0.001) and vasoactive intestinal peptide (148% of normal, P < 0.05). Furthermore, CF pancreatic cAMP levels were 147% of normal (P < 0.01). These data suggest that the CF pancreas may be chronically stimulated by cAMP-mediated signals, which in turn may exacerbate protein plugging in the acinar/ductal lumen, believed to be the primary cause of destruction of the pancreas in CF.
amylase; bicarbonate ion; adenosine 3',5'-cyclic monophosphate; cystic fibrosis; Muclin; secretin; vasoactive intestinal peptide
This article has been cited by other articles:
![]() |
B. S. Magenheimer, P. L. St. John, K. S. Isom, D. R. Abrahamson, R. C. De Lisle, D. P. Wallace, R. L. Maser, J. J. Grantham, and J. P. Calvet Early Embryonic Renal Tubules of Wild-Type and Polycystic Kidney Disease Kidneys Respond to cAMP Stimulation with Cystic Fibrosis Transmembrane Conductance Regulator/Na+,K+,2Cl- Co-Transporter-Dependent Cystic Dilation J. Am. Soc. Nephrol., December 1, 2006; 17(12): 3424 - 3437. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. S. Stalvey, C. Muller, D. A. Schatz, C. H. Wasserfall, M. L. Campbell-Thompson, D. W. Theriaque, T. R. Flotte, and M. A. Atkinson Cystic Fibrosis Transmembrane Conductance Regulator Deficiency Exacerbates Islet Cell Dysfunction After {beta}-Cell Injury. Diabetes, July 1, 2006; 55(7): 1939 - 1945. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. J. C. Bijvelds, I. Bronsveld, R. Havinga, M. Sinaasappel, H. R. de Jonge, and H. J. Verkade Fat absorption in cystic fibrosis mice is impeded by defective lipolysis and post-lipolytic events Am J Physiol Gastrointest Liver Physiol, April 1, 2005; 288(4): G646 - G653. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Norkina, T. G. Burnett, and R. C. De Lisle Bacterial Overgrowth in the Cystic Fibrosis Transmembrane Conductance Regulator Null Mouse Small Intestine Infect. Immun., October 1, 2004; 72(10): 6040 - 6049. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Kaur, O. Norkina, D. Ziemer, L. C. Samuelson, and R. C. De Lisle Acidic duodenal pH alters gene expression in the cystic fibrosis mouse pancreas Am J Physiol Gastrointest Liver Physiol, August 1, 2004; 287(2): G480 - G490. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Norkina, S. Kaur, D. Ziemer, and R. C. De Lisle Inflammation of the cystic fibrosis mouse small intestine Am J Physiol Gastrointest Liver Physiol, June 1, 2004; 286(6): G1032 - G1041. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. C. De Lisle Role of sulfated O-linked glycoproteins in zymogen granule formation J. Cell Sci., July 15, 2002; 115(14): 2941 - 2952. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |