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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Influence of gastrointestinal (GI) hormones on suckling, gastric emptying and pancreatic trypsin content in the developing rat.

Aim of this study was to investigate how gastrointestinal hormones such as exogenous s.c. caerulein (6 micrograms/kg body weight), secretin (100 U/kg body weight), bombesin (20 micrograms/kg body weight, s.c.), CCK-8 (10 micrograms/kg body weight, i.p.), the CCK-A receptor antagonist L 364,718 (100 micrograms/kg body weight, i.p.), camostate (400 mg/kg body weight per os) which releases endogenous CCK and the coadministration of camostate with atropin (250 micrograms/kg body weight, s.c) or L 364,718 (1 mg/kg) influence milk intake from nipples, gastric emptying, and discharge of pancreatic trypsin content in 10-day-old rat pups. Saline-treated pups served as controls. The non-fasting Wistar rat pups of both sexes were used in littermate order. The suckling lasted for 30 and 45 min, respectively. One pup was used only once. After suckling the pups were decapitated, their stomach and pancreas were removed and weighed. The gastric food content was regarded as intake of milk and expressed as difference between the filled minus empty stomach. Pancreatic trypsin and protein content, plasma CCK level were measured. The exogenous agents did not influence gastric content. The investigated peptides decreased, L 364,718, however, increased the pancreatic trypsin/protein ratio. Camostate increased gastric content by 60% and decreased pancreatic trypsin/protein ratio vs saline by 90%. The gastric and pancreatic effects of camostate were not reversed by atropine or L 364,718. Conclusion: Exogenous and endogenous CCK seem not to influence milk intake while decrease pancreatic trypsin/protein ratio. However, endogenous CCK inhibit gastric emptying. The plasma CCK level was elevated due to the applied CCK-8 and camostate during the observed suckling period.[1]

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