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Time-course of the pancreatic changes following long-term stimulation or inhibition of the CCK-A receptor

Ohlsson, Bodil LU ; Axelson, Jan LU ; Sternby, Berit LU ; Rehfeld, Jens F and Ihse, Ingemar LU (1995) In International Journal of Pancreatology 18(1). p.59-66
Abstract
Cholecystokinin (CCK) reportedly induces both hyperplastic and hypertrophic changes in the pancreas. Blockade of the CCK receptor results in decreased pancreatic secretion and atrophy. The aim of this study was to evaluate the time-course of the effects of stimulation and inhibition of the CCK-A receptor in the rat exocrine pancreas. Male rats had infusion of sulfated CCK-8, the CCK-A receptor antagonist devazepide, or sodium chloride by osmotic minipumps. After 36 h, 3, 7, or 28 d the rats had ip injections of thymidine, and 1 h later they were sacrificed. The pancreas was excised, weighed, and its content of protein, DNA, water, and enzymes was analyzed. Histologic samples were prepared for autoradiography. Pancreatic weight, protein,... (More)
Cholecystokinin (CCK) reportedly induces both hyperplastic and hypertrophic changes in the pancreas. Blockade of the CCK receptor results in decreased pancreatic secretion and atrophy. The aim of this study was to evaluate the time-course of the effects of stimulation and inhibition of the CCK-A receptor in the rat exocrine pancreas. Male rats had infusion of sulfated CCK-8, the CCK-A receptor antagonist devazepide, or sodium chloride by osmotic minipumps. After 36 h, 3, 7, or 28 d the rats had ip injections of thymidine, and 1 h later they were sacrificed. The pancreas was excised, weighed, and its content of protein, DNA, water, and enzymes was analyzed. Histologic samples were prepared for autoradiography. Pancreatic weight, protein, and DNA were increased at 36 h after the start of CCK infusion and throughout the study period. CCK stimulation also increased the content of trypsin at days 3 and 28. The labeling index of pancreatic acinar cells was increased at 36 h. Blockade of endogenous CCK by the receptor antagonist devazepide led to decreased pancreatic weight from the third day of infusion, whereas the protein content was decreased from the seventh day. At day 28, the DNA content was decreased by devazepide. However, the labeling index of acinar cells decreased transiently already at 36 h. Neither CCK nor devazepide caused any changes of protein content:DNA content ratio during the study. Continuous infusion of CCK caused pancreatic hyperplasia already after 36 h. Stimulation up to 28 d did not cause any further effects. The adverse changes found after blockade of the CCK-A receptor showed much of the same time-course. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Cholecystokinin, devazepide, pancreas, trophic effects
in
International Journal of Pancreatology
volume
18
issue
1
pages
59 - 66
publisher
Humana Press
external identifiers
  • pmid:7594771
  • scopus:0029125821
ISSN
0169-4197
DOI
10.1007/BF02825422
language
English
LU publication?
yes
id
0c220a03-84a2-4a20-8c01-42de4dee1158 (old id 1109167)
date added to LUP
2008-07-25 14:41:42
date last changed
2017-01-01 07:18:44
@article{0c220a03-84a2-4a20-8c01-42de4dee1158,
  abstract     = {Cholecystokinin (CCK) reportedly induces both hyperplastic and hypertrophic changes in the pancreas. Blockade of the CCK receptor results in decreased pancreatic secretion and atrophy. The aim of this study was to evaluate the time-course of the effects of stimulation and inhibition of the CCK-A receptor in the rat exocrine pancreas. Male rats had infusion of sulfated CCK-8, the CCK-A receptor antagonist devazepide, or sodium chloride by osmotic minipumps. After 36 h, 3, 7, or 28 d the rats had ip injections of thymidine, and 1 h later they were sacrificed. The pancreas was excised, weighed, and its content of protein, DNA, water, and enzymes was analyzed. Histologic samples were prepared for autoradiography. Pancreatic weight, protein, and DNA were increased at 36 h after the start of CCK infusion and throughout the study period. CCK stimulation also increased the content of trypsin at days 3 and 28. The labeling index of pancreatic acinar cells was increased at 36 h. Blockade of endogenous CCK by the receptor antagonist devazepide led to decreased pancreatic weight from the third day of infusion, whereas the protein content was decreased from the seventh day. At day 28, the DNA content was decreased by devazepide. However, the labeling index of acinar cells decreased transiently already at 36 h. Neither CCK nor devazepide caused any changes of protein content:DNA content ratio during the study. Continuous infusion of CCK caused pancreatic hyperplasia already after 36 h. Stimulation up to 28 d did not cause any further effects. The adverse changes found after blockade of the CCK-A receptor showed much of the same time-course.},
  author       = {Ohlsson, Bodil and Axelson, Jan and Sternby, Berit and Rehfeld, Jens F and Ihse, Ingemar},
  issn         = {0169-4197},
  keyword      = {Cholecystokinin,devazepide,pancreas,trophic effects},
  language     = {eng},
  number       = {1},
  pages        = {59--66},
  publisher    = {Humana Press},
  series       = {International Journal of Pancreatology},
  title        = {Time-course of the pancreatic changes following long-term stimulation or inhibition of the CCK-A receptor},
  url          = {http://dx.doi.org/10.1007/BF02825422},
  volume       = {18},
  year         = {1995},
}