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The trophic effect of cholecystokinin on the pancreas declines in rats on total parenteral nutrition
Author(s) -
Wu XM.,
Liao YW.,
Ji KQ.,
Li GF.,
Zang B.
Publication year - 2012
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/j.1439-0396.2011.01140.x
Subject(s) - cholecystokinin , medicine , pancreas , endocrinology , atrophy , exocrine pancreas , parenteral nutrition , cholecystokinin receptor , antagonist , gastrointestinal hormone , biology , receptor , peptide hormone
Summary Total parenteral nutrition (TPN) results in atrophy of the pancreas, while cholecystokinin (CCK) can significantly stimulate the exocrine pancreas in rodents. This study was designed to examine whether CCK may improve the atrophy of the pancreas in rats on TPN treatment. Forty‐eight Sprague–Dawley rats were divided into orally fed and TPN groups and were infused with CCK at a dose of 5 μg/kg/h or the CCK‐receptor antagonist devazepide at a dose of 200 μg/kg/h for 10 days. Infusion of CCK caused hypercholecystokininemia (hyperCCKemia) and decreased the atrophy of the pancreas resulting from TPN. The hyperplastic response to CCK in orally fed rats was decreased in the rats given TPN. Devazepide did not influence the pancreatic variables. This study further confirmed that CCK stimulates the exocrine pancreas and decreases the atrophy of the exocrine pancreas resulting from TPN. Our present findings suggest that the trophic effect of CCK on the exocrine pancreas declines in TPN.