The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

Nylander, Anna‐Greta; Chen, Duan; Ding, Xi‐Qin; Norlén, Per; Håkanson, R.

doi:10.1111/j.1600-0773.1997.tb00387.x

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…an important physiological role both in the meal-induced release of pancreatic enzymes and in the regulation of pancreatic growth (10,30,33,37), the influence of vagotomy on the pancreatic growth is still controversial (2,5,16,26,27,39,41).…”

mentioning

confidence: 99%

Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats

Yamamoto

Otani

Jia

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Recent studies demonstrated that cholecystokinin (CCK) at physiological levels stimulates pancreatic enzyme secretion via a capsaicin-sensitive afferent vagal pathway. This study examined whether chemical ablation of afferent vagal fibers influences pancreatic growth and secretion in rats. Bilateral subdiaphragmatic vagal trunks were exposed, and capsaicin solution was applied. Pancreatic wet weight and pancreatic secretion and growth in response to endogenous and exogenous CCK were examined 7 days after capsaicin treatment. Perivagal application of capsaicin increased plasma CCK levels and significantly increased pancreatic wet weight compared with those in the control rats. Oral administration of CCK-1 receptor antagonist loxiglumide prevented the increase in pancreatic wet weight after capsaicin treatment. In addition, continuous intraduodenal infusion of trypsin prevented the increase in plasma CCK levels and pancreatic wet weight after capsaicin treatment. There were no significant differences in the expression levels of CCK-1 receptor mRNA and protein in the pancreas in capsaicin-treated and control rats. Intraduodenal administration of camostat or intravenous infusion of CCK-8 stimulated pancreatic secretion in control rats but not in capsaicin-treated rats. In contrast, repeated oral administrations of camostat or intraperitoneal injections of CCK-8 significantly increased pancreatic wet weight in both capsaicin-treated and control rats. Present results suggest that perivagal application of capsaicin stimulates pancreatic growth via an increase in endogenous CCK and that exogenous and endogenous CCK stimulate pancreatic growth not via vagal afferent fibers but directly in rats.

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mentioning

confidence: 99%

Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats

Yamamoto

Otani

Jia

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Circulating CCK does not seem to stimulate pancreatic growth under physiological conditions but appears to be essential for the maintenance of the pancreas [4]. High doses of CCK induce pancreatic hyperplasia/hypertrophy [4] and pancreatitis in rats [2].…”

Section: Effects Of Ethanolmentioning

confidence: 99%

“…This hormone, which is released from cells in the mucosa of the duodenum-jejunum in response to fat and protein in the lumen [3], induces pancreatic hypertrophy and hyperplasia in experimental animals [4]. In fact, administration of large doses of CCK can induce pancreatitis [2].…”

Section: Introductionmentioning

confidence: 99%

Effects of Daily Fat or Ethanol Ingestion on the Cholecystokinin- Pancreas and the Gastrin- Enterochromaffin-Like Cell Axes in Rats

Yamada¹,

Kimura²,

Chen³

1998

Digestion

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Background/Aims: Ingestion of fat and ethanol is thought to contribute to the development of pancreatitis through the release of gut hormones, such as cholecystokinin (CCK) and gastrin. We have examined the effects of fat or ethanol on the relationships between CCK and pancreas on one hand and between gastrin and the enterochromaffin-like (ECL) cells in the stomach on the other. Methods: In one study, rats received 2 ml of medium-chain triglycerides or water twice a day by the oral route for 12 days. In another study, rats received 2.5, 5, 10 or 20% ethanol in drinking water for 12 days. All rats were killed on day 13. Results: There were no changes in either the plasma CCK concentration or the pancreatic weight and DNA content in the fat-fed rats. The serum gastrin concentration and the histidine decarboxylase (HDC) activity, HDC mRNA level and histamine content of the ECL cells were lower in fat-fed rats than in control rats. Ethanol did not affect either the plasma CCK concentration or the pancreatic weight and DNA content. The serum gastrin concentration was reduced in the rats that received 5, 10 or 20% ethanol. Also the HDC activity and histamine content of the ECL cells were reduced in the rats that received 10 and 20% ethanol. Conclusion: Daily ingestion of fat or ethanol for 12 days was without effects on the plasma CCK concentration and the pancreas, but reduced the serum gastrin concentration and the activity of the ECL cells in the rat.

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Cholecystokinin-producing (I) cells of intestinal mucosa in dexamethasone-treated rats

Koko

Cvijic̀

Milošević

et al. 2011

Regulatory Peptides

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The Trophic Response of Rat Pancreas to Sulfated Cholecystokinin‐8 is Dose‐ and Time‐Dependent and Not Affected by Vagotomy or Atropine

Cited by 3 publications

References 38 publications

Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats

Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats

Effects of Daily Fat or Ethanol Ingestion on the Cholecystokinin- Pancreas and the Gastrin- Enterochromaffin-Like Cell Axes in Rats

Cholecystokinin-producing (I) cells of intestinal mucosa in dexamethasone-treated rats

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