Endogenous Cholecystokinin Release Responsible for Pancreatic Growth Observed after Pancreatic Juice Diversion*

Rivard, Nathalie; Guan, Difu; Maouyo, Djikolngar; Grondin, Gilles; Bérubé, France-Line; Morisset, Jean

doi:10.1210/endo-129-6-2867

Cited by 36 publications

(18 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, as octreotide already affected the endocrine and exocrine pancreas at much lower doses, reduced food intake alone cannot explain our results. This is in agreement with an observation of Rivard et al (1991 a). Second, octreotide must have inhibited camostate-induced release of endogenous CCK in our study (Schmidt et al 1989).…”

Section: Discussionsupporting

confidence: 94%

Rat pancreas after long‐term treatment with the somatostatin analogue octreotide

Schönfeld¹,

Meisse²,

Muller³

1995

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYSomatostatin is a potent inhibitor of endocrine and exocrine pancreatic secretion. However, it is not clear whether it also inhibits pancreatic growth. Therefore we treated male Wistar rats with a somatostatin analogue, octreotide ,tg/(kg body wt.day)), over a period of 14 days. In a dose-dependent manner, this potent and long-acting analogue caused a reduction in weight of the pancreas and a reduction in pancreatic content of protein, DNA, trypsin, chymotrypsin, amylase and lipase, as well as pancreatic content of insulin-, glucagon-and somatostatin-like immunoreactivities. When growth of rat pancreas was induced by oral administration of camostate (200 mg/(kg body wt.day) or by subcutaneous administration of cholecystokinin (2 x 10 /tg/(kg body wt.day)) over a period of 14 days, octreotide ,ug/(kg body wt.day)) had the same effects, but these were even more pronounced. We conclude that somatostatin is an important regulator of pancreatic growth.

show abstract

Section: Discussionsupporting

confidence: 94%

Rat pancreas after long‐term treatment with the somatostatin analogue octreotide

Schönfeld¹,

Meisse²,

Muller³

1995

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…This trophic action of CCK can be obtained whether CCK was exogenously administered (Solomon et al 1983) or endogenously released either by feeding a high-protein diet (Morisset et al 1992) or following pancreatic juice diversion (Rivard et al 1991) and CCK exerts this trophic effect, not via a vagal afferent pathway, but directly on the pancreas, in vivo (Yamamoto et al 2003). In each situation, the CCK 1 receptor implicated as the response to CCK was abolished by the specific CCK 1 receptor antagonist L-364,718 (Rivard et al 1991;Morisset et al 1992) Moreover, CCK and gastrin are implicated in the growth of the exocrine pancreas by causing hypertrophy and hyperplasia (Baldwin, 1995) and increasing DNA, RNA and the protein contents of rat pancreas (Johnson, 1981). Administration of CCK8 caused both increased proliferation and apoptosis in the pancreas.…”

Section: Global Effects Of Gastrin and Cholecystokinin In The Gutmentioning

confidence: 99%

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

et al. 2006

Self Cite

View full text Add to dashboard Cite

The aim of the present review is to synthesise and summarise our recent knowledge on the involvement of cholecystokinin (CCK) and gastrin peptides and their receptors in the control of digestive functions and more generally their role in the field of nutrition in mammals. First, we examined the release of these peptides from the gut, focusing on their molecular forms, the factors regulating their release and the signalling pathways mediating their effects. Second, general physiological effects of CCK and gastrin peptides are described with regard to their specific receptors and the role of CCK on vagal mucosal afferent nerve activities. Local effects of CCK and gastrin in the gut are also reported, including gut development, gastrointestinal motility and control of pancreatic functions through vagal afferent pathways, including NO. Third, some examples of the intervention of the CCK and gastrin peptides are exposed in diseases, taking into account intervention of the classical receptor subtypes (CCK 1 and CCK 2 receptors) and their heterodimerisation as well as CCK-C receptor subtype. Finally, applications and future challenges are suggested in the nutritional field (performances) and in therapy with regards to the molecular forms or in relation with the type of receptor as well as new techniques to be utilised in detection or in therapy of disease. In conclusion, the present review underlines recent developments in this field: CCK and gastrin peptides and their receptors are the key factor of nutritional aspects; a better understanding of the mechanisms involved may increase the efficiency of the nutritional functions and the treatment of abnormalities under pathological conditions.

show abstract

“…Oral administration of soybean trypsin inhibitor (5,44) or the synthetic protease inhibitor camostat (10,15,37,52,55), as well as pancreaticobiliary diversion (13,39), increase the release of endogenous CCK into the blood and induce pancreatic growth. Moreover, CCK-A receptor antagonists that block the action of exogenous and endogenous CCK inhibit pancreatic growth (10,13,37,39,52). Therefore, most of the studies of pancreatic growth have been focused on CCK as a key regulator.…”

mentioning

confidence: 99%

Calcineurin mediates pancreatic growth in protease inhibitor-treated mice

Tashiro¹,

Samuelson²,

Liddle³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

. Calcineurin mediates pancreatic growth in protease inhibitor-treated mice. Am J Physiol Gastrointest Liver Physiol 286: G784-G790, 2004. First published December 18, 2003 10.1152/ ajpgi.00446.2003.-CCK acts on pancreatic acinar cells to increase intracellular Ca 2ϩ leading to secretion of digestive enzymes and, in the long term, pancreatic growth. Calcineurin (CN) is a serine/ threonine-specific protein phosphatase activated by Ca 2ϩ and calmodulin that recently has been shown to participate in the growth regulation of cardiac and skeletal myocytes. We therefore tested the effect of two different CN inhibitors, cyclosporine A (CsA) and FK506, on mouse pancreatic growth induced by oral administration of the synthetic protease inhibitor camostat, a known stimulator of endogenous CCK release. Mice were fed a powdered diet with or without 0.1% camostat. Pancreatic wet weight, protein, and DNA were increased in response to camostat in a time-dependent manner over 10 days in ICR mice but not in CCK-deficient mice. Both CsA (15 mg/kg) and FK506 (3 mg/kg) given twice daily blocked the increase in pancreatic wet weight and protein and DNA content induced by camostat. The increase in plasma CCK induced by camostat was not blocked by CsA or FK506. Camostat feeding also increased the relative amount of CN protein, whereas levels of MAPKs, ERKs, and p38 were not altered. In summary, 1) CCK released by chronic camostat feeding induces pancreatic growth in mice; 2) this growth is blocked by treatment with both CsA and FK506, indicating a role for CN; 3) CCK stimulation also increases CN protein. In conclusion, activation and possibly upregulation of CN may participate in regulation of pancreatic growth by CCK in mice.cholecystokinin; camostat; FK506; cyclosporine A A VARIETY OF GASTROINTESTINAL peptides have been implicated in the regulation of proliferation and differentiation in the mature gastrointestinal tract and the pancreas (30,56). It is well known that feeding initiates pancreatic protein synthesis and secretion and that adaptation to a high-protein diet results in pancreatic growth (17, 18). More detailed studies have shown that among gastrointestinal peptides, CCK is released in response to dietary protein leading to pancreatic growth. Injection of CCK increases pancreatic wet weight and protein and DNA content in vivo over 4-10 days (8,37,40,43). Oral administration of soybean trypsin inhibitor (5, 44) or the synthetic protease inhibitor camostat (10,15,37,52,55), as well as pancreaticobiliary diversion (13, 39), increase the release of endogenous CCK into the blood and induce pancreatic growth. Moreover, CCK-A receptor antagonists that block the action of exogenous and endogenous CCK inhibit pancreatic growth (10, 13, 37, 39, 52). Therefore, most of the studies of pancreatic growth have been focused on CCK as a key regulator.In pancreatic acinar cells, the intracellular mechanisms of enzyme secretion have been well documented. CCK activates the release of intracellular Ca 2ϩ and the influx of Ca 2ϩ and generate...

show abstract

Endogenous Cholecystokinin Release Responsible for Pancreatic Growth Observed after Pancreatic Juice Diversion*

Cited by 36 publications

References 35 publications

Rat pancreas after long‐term treatment with the somatostatin analogue octreotide

Rat pancreas after long‐term treatment with the somatostatin analogue octreotide

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

Calcineurin mediates pancreatic growth in protease inhibitor-treated mice

Contact Info

Product

Resources

About