Long‐term comparative effect of cholecystokinin and gastrin on mouse stomach, antrum, intestine, and exocrine pancreas

Abstract

Mice were injected three times a day for 12 days with 300 micrograms/kg body weight of gastrin G17 or 37.5 Ivy dog U/kg body weight of CCK or saline. Other mice were also injected four times an hr for 1 hr with 7.5 micrograms/kg of gastrin, nine Ivy dog U/kg of CCK or saline; 1 hr before killing, they were injected with tritiated thymidine to evaluate the labelling indices in peptic, antral, duodenal, jejunal, and ileal mucosae. Four hours after the first injection of the two peptides, the peptic labelling indices increased while those of intestinal mucosa increased 8 hr after these injections. Long-term injections of CCK had a trophic effect on secretory cells of the digestive tract: the number of gastric zymogenic cells, Paneth cells, and the mucous cells of Brünner glands were hypertrophied. The pepsin, amylase, chymotrypsin, and lysozyme activities increased in stomach, exocrine pancreas, and intestine, respectively. Neither parietal cells nor intestinal enterocytes and hydrolase activities were affected. The trophic effect of long-term injections of gastrin is confirmed on parietal cells and exocrine pancreatic parenchyma and is demonstrated in Paneth cells. Confirming cytological results, pancreatic lipase and amylase activities and intestinal lysozyme activity were increased after gastrin. Although CCK and gastrin have a structural analogy, these two peptides did not affect the same cellular types. A specific action of CCK on the main secretory cells of the digestive mucosa is demonstrated.

Diet Supplemented with Yoghurt or Milk Fermented by <i>Lactobacillus casei</i> DN-114 001 Stimulates Growth and Brush-Border Enzyme Activities in Mouse Small Intestine

“…Pentagastrin, continuously infused into the duodenal lumen of the conscious rat [33], increased intestinal epithelial cell proliferation, villous area, Paneth cell number and aminopeptidase and alkaline phosphatase-specific activities. Furthermore, intraperitoneal injections of gastrin (G17) or cholecystokinin also had transient trophic effects on mouse intestinal epithelium proliferation that partly disappeared after 12 days of injection [17].…”

“…All studies were carried out without access to the histological fragments coding. Variations of the villous area were evaluated at the three levels of the small intestine, as already described [17]. For each segment, the ratio of mucosal surface area to the corresponding serosal surface area was calculated, giving the increasing rate of the absorbing surface by the intestinal villi (Irv) (10 micrographs/intestinal level/animal).…”

Autocrine stimulation of growth of AR4-2J rat pancreatic tumour cells by gastrin

“…Gastrin, amongst its range of physiological actions, is a trophic factor for the normal gastrointestinal mucosa (Enochs & Johnson, 1977;Balas et al, 1985). There is increasing evidence that gastrin is also a growth factor for gastric and colonic cancers in vivo.…”

Pancreatic Growth after Pancreatico-Biliary Diversion Does Not Increase the Capacity to Secrete Amylase

“…High doses of cerulein given to freely fed rats depleted the enzyme stores of amylase, chymotrypsin and lipase with 80-90% within 3 h, and amylase synthesis remained low during 3 days of maximal stimulation [27]. CCK and cerulein increase the content and concentration of pancreatic enzymes in fasted or starved rats [8,10], with an increased zymogen volume fraction [7]. In fasted rats, CCK increases the pancreatic content of amylase and trypsin, but not lipase [4].…”

“…Repeated injections of CCK or its analogue cerulein induce trophic effects in the pancreas [5][6][7][8], which could also be seen during continuous endogenous or exogenous hyperCCKemia [9]. The exogenous stimulation of the pancreas results in increased contents of amylase, lipase, and chymotrypsin in fasted or starved rats [7,8,10]. Thus, trophic stimuli increase pancreatic enzyme synthesis, which is also suggested by the increased transcription of genes for enzymes after pancreatico-biliary diversion (PBD) [10].…”