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1 Department of Physiology, The University of Michigan, Ann Arbor, Michigan 48109-0622; and 2 Department of Clinical Biochemistry Rigshospitalet, DK 2100 Copenhagen, Denmark
A CCK-deficient
mouse mutant generated by gene targeting in embryonic stem cells was
analyzed to determine the importance of CCK for growth and function of
the exocrine pancreas and for pancreatic adaptation to dietary changes.
RIAs confirmed the absence of CCK in mutant mice and demonstrated that
tissue concentrations of the related peptide gastrin were normal.
CCK-deficient mice are viable and fertile and exhibit normal body
weight. Pancreas weight and cellular morphology appeared normal,
although pancreatic amylase content was elevated in CCK-deficient mice.
We found that a high-protein diet increased pancreatic weight, protein,
DNA, and chymotrypsinogen content similarly in CCK-deficient and
wild-type mice. This result demonstrates that CCK is not required for
protein-induced pancreatic hypertrophy and increased proteolytic enzyme
content. This is a novel finding, since CCK has been considered the
primary mediator of dietary protein-induced changes in the pancreas.
Altered somatostatin concentrations in brain and duodenum of
CCK-deficient mice suggest that other regulatory pathways are modified
to compensate for the CCK deficiency.
gastrointestinal hormones; knockout mice; acinar cells; digestive enzymes; pancreatic hypertrophy
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