Key result
Cholecystokinin infusion (5 μg/kg/h) decreased pancreatic atrophy resulting from total parenteral nutrition in rats, though its trophic effect declined compared to orally fed rats.
Why the study?
Does cholecystokinin improve the atrophy of the pancreas in rats on total parenteral nutrition?
Does cholecystokinin improve the atrophy of the pancreas in rats on total parenteral nutrition?
CCK decreases TPN-induced pancreatic atrophy, but its trophic effect is blunted compared to orally fed rats.
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.
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Wu et al. (2011) studied Pancreatic atrophy from total parenteral nutrition (n=48). Cholecystokinin (CCK) vs. Orally fed rats and devazepide (200 μg/kg/h) was evaluated on Pancreatic atrophy and hyperplastic response. Cholecystokinin infusion (5 μg/kg/h) decreased pancreatic atrophy resulting from total parenteral nutrition in rats, though its trophic effect declined compared to orally fed rats.
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