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

Balas, D; Senegas-Balas, F.; Pradayrol, Lucien; Vayssette, Jacqueline; Bertrand, C.; Ribet, A

doi:10.1002/aja.1001740104

Cited by 47 publications

(18 citation statements)

References 60 publications

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“…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].…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

Section: Histological and Morphological Studiesmentioning

confidence: 99%

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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

Thoreux¹,

Balas²,

Bouley

et al. 1998

Digestion

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The nutritional benefits of lactic acid bacteria in fermented dairy products have been well documented, especially in terms of weight gain and feed efficiency, but not in terms of small intestine adaptation. The effects of a diet supplemented (30% wt/wt) with milk fermented either by Lactobacillus casei DN-114 001 or yoghurt for 3 or 15 days were investigated in the small intestine of mice by morphometry, kinetic analysis and determination of brush-border enzyme activities. Results were compared with those obtained with standard or milk isocaloric diets. Cell proliferation and villous area were significantly increased in the proximal intestine of mice fed the fermented-milk-supplemented diets for 3 days and were associated with hypertrophy and hyperplasia of Paneth and goblet cells. Lactase-specific activity was increased by fermented-milk diets at days 3 and 15, whereas there was no variation in maltase-specific activity. Alkaline phosphatase-specific activity was increased after 3 days of the three tested diets in the whole intestine, and after 15 days in the proximal intestine. Aminopeptidase activity was increased in the distal part of the intestine after 3 days of the 3 diets. Our findings suggest that diets supplemented with fermented milks have a positive effect on the trophicity of the mucosa in the small intestine of mice.

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Section: Discussionmentioning

confidence: 99%

Section: Histological and Morphological Studiesmentioning

confidence: 99%

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

Thoreux¹,

Balas²,

Bouley

et al. 1998

Digestion

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“…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.…”

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confidence: 99%

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

Blackmore

Bh²

1992

Br J Cancer

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Summary The control of cell proliferation by gastrin has been investigated in a rat pancreatic tumour cell line, AR4-2J. Exogenous gastrin, 10-12 to 10-8 M, stimulated cell growth of thymidine-synchronised AR4-2J cells cultured over 48 h in serum-free medium. Cell lysates of AR4-2J cells contained an average of 4.5 and 3.5 pg gastrin per 106 cells, when grown in serum-supplemented or serum-free media, respectively, as revealed by radioimmunoassay. In serum-free medium, AR4-2J secrete 34ngl 10-6 cells of gastrin over 48h. Addition of an anti-gastrin immunoglobulin preparation, but not control immunoglobulins, caused a maximum 52% reduction in cell growth. These data are consistent with an autocrine role for gastrin in the control of AR4-2J cell growth. These results were supported by studies with gastrin/CCK receptor antagonists. Six non-peptide gastrin/CCK receptor antagonists inhibited AR4-2J cell growth in a concentration-related manner. The concentration required for 50% inhibition (IC50) of cell growth by the amino acid-derived antagonists proglumide (3.5 x 10-M), benzotript (1.8 x 10-3 M), loxiglumide (1.1 x 10-4 M) and lorglumide (6.7 x 10-5 M) were of the same order and significantly correlated with their IC50 for inhibition of 1251-gastrin binding to AR4-2J cells. Inhibition of cell growth by these antagonists was partially reversed by the addition of exogenous gastrin. In contrast, the ICm for inhibition of cell growth with two benzodiazepine-derived antagonists, the CCK-B receptor antagonist L-365,260 (4.6 x 10-5 M) and the CCK-A receptor antagonist devazepide (1.7 x 10-' M) were two-three orders of magnitude greater than those required to inhibit gastrin binding (10-8-10-7 M). The growth inhibitory effects of L-365,260 and devazepide were not reversed by exogenous gastrin suggesting these benzodiazepine-derived antagonists do not inhibit cell growth by interaction with gastrin receptors. The results are consistent with gastrin being an autocrine growth factor in AR4-2J cells, and that stimulation of cell growth is due to stimulation of the gastrin, rather than CCK-B, receptor sub-type. This study highlights that gastrin receptor antagonists warrant further investigation as agents to control growth of tumours, such as those from the gastrointestinal tract, which express gastrin receptors.

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“…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].…”

Section: Discussionmentioning

confidence: 99%

“…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].…”

mentioning

confidence: 99%

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

Axelson¹,

Jansen²,

Sternby

et al. 1999

Eur Surg Res

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Background/Aim: Cholecystokinin (CCK) stimulates secretion and evokes a hyperplastic response in the rat pancreas. The aims of this study were to measure the effect of chronic hyperCCKemia induced by pancreatico-biliary diversion (PBD) on pancreatic enzyme concentrations, on amylase secretion by dispersed acinar cells, and on the CCK-stimulated secretion of pancreatic juice in PBD-operated rats. Material and Methods: Forty-five Sprague-Dawley male rats had either PBD or sham operation 4 weeks before sacrifice or additional experiments. In the first study, 25 rats (13 PBD and 12 sham-operated rats) were either freely fed or fasted overnight before sacrifice. The pancreas was dissected out, weighed and analyzed. In the second study, the rats (6 PBD and 7 sham-operated rats) were fasted overnight before pancreatic acini were prepared. Secretion of amylase during stimulation of acini with CCK-8S and carbachol was measured. In the third study (5 sham-operated and 4 PBD rats), the rats were fasted overnight before basal and CCK-stimulated secretion was measured in vivo. Results: PBD-operated rats showed a threefold increase in pancreatic wet weight with increased contents of DNA, protein and water. The concentration of pancreatic amylase was 7–12% of that found in control animals. The concentrations of trypsin and lipase were also lowered. Stimulation of dispersed pancreatic acini with CCK-8S or carbachol resulted in secretion of amylase to a similar extent in PBD and sham-operated rats. There was no difference in the secretion of pancreatic juice in response to CCK, but although the output of amylase from PBD-operated rats increased with CCK, it remained at a low level throughout the study period. Conclusion: PBD evoked hyperplastic changes in the rat pancreas and decreased the concentrations of amylase, trypsin and lipase. However, the capacity of acinar cells to secrete amylase remained intact. The stimulated pancreatic secretion was not changed in volume, but the output of amylase was low in PBD-operated rats. The findings are consistent with the idea that the enlargement of the pancreas following PBD does not improve the secretory capacity.

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

Cited by 47 publications

References 60 publications

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

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

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

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

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