Pancreatic Secretion and the Release of Cholecystokinin after a Meal in Dogs with and without Exclusion of Pancreatic Juice

Kogire, Masafumi; Inoue, Kayo; Hosotani, Ryo; Huang, Yuesheng; Thompson, James C.; Tobe, Takayoshi

doi:10.3109/00365528909093081

Cited by 7 publications

(3 citation statements)

References 17 publications

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“…Therefore in dogs CCK does not seem to mediate the putative feedback mechanism between intraluminal protease and pancreatic enzyme secretion. Our results are consistent with the report of Kogire et al [9] who also denied the existence of a CCKmediated feedback regulation in dogs, based on their pancreatic juice exclusion studies.…”

Section: Discussionsupporting

confidence: 83%

“…Inconclu sive results have been reported from studies in dogs. Although a number of authors could not confirm a feedback regulation of exocrine pancreatic secretion by CCK in dogs [7][8][9], Inoue et al [10] reported an increased release of CCK after pancreatic duct ligation, and Hosotani et al [15] described the inhibition of postprandial pancreatic enzyme secretion by a potent CCK receptor antagonist. There fore we performed an experimental study in dogs in which this matter was studied in a different model.…”

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confidence: 99%

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Postprandial Release of Cholecystokinin after Duodenum-Preserving Total Pancreatectomy Is Independent of Intraluminal Pancreatic Protease Activity in Dogs

Guicherit¹,

Gooszen²,

Jansen³

et al. 1990

Digestion

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The effect of meal stimulation, with and without the intraduodenal presence of pancreatic enzymes, on plasma cholecystokinin (CCK) release was studied in order to investigate the role of CCK in the putative feedback mechanism between intraduodenal pancreatic proteases and pancreatic enzyme secretion. Plasma CCK concentrations in response to a semiliquid meal, with and without the supplementation of exocrine pancreatic enzymes, were measured in 8 dogs after duodenum preserving pancreatectomy. With a well-balanced endocrine and exocrine substitution regimen all dogs were kept in good clinical condition, without steatorrhea or significant weight loss, and fasting plasma glucose levels within the normal range. Exocrine supplementation was stopped at least 3 days prior to tests. Basal plasma CCK levels after 3 days without exocrine supplementation (2.5 ± 0.3 pM) did not significantly differ from the results with supplementation (3.0 ± 0.5 pM) nor from the pre-operative levels (2.3 ± 0.3 pM). In addition, integrated plasma CCK responses to the meal without exocrine supplementation (330 ± 37 pM•90min) were not significantly different from the responses to the meal with exocrine supplementation (303 ± 49 pM•90 min), or from the postprandial CCK response in the dogs with an intact pancreas preoperatively (390 ± 100 pM 90 min). It is concluded that the release of CCK in dogs after total pancreatectomy is independent of intraluminal protease activity. It is therefore not likely that CCK mediates the putative feedback mechanism between intraluminal protease activity and pancreatic enzyme secretion in dogs.

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Section: Discussionsupporting

confidence: 83%

mentioning

confidence: 99%

Postprandial Release of Cholecystokinin after Duodenum-Preserving Total Pancreatectomy Is Independent of Intraluminal Pancreatic Protease Activity in Dogs

Guicherit¹,

Gooszen²,

Jansen³

et al. 1990

Digestion

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“…Important basic information regarding the physiology of the exocrine pancreas has been derived from studies in dogs. However, it is disputed whether the feedback mechanism observed in rats and postulated in humans also exists in dogs (10)(11)(12)(13). The latter are not considered appropriate experimental animals for such investigations.…”

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confidence: 95%

Feedback Regulation of Exocrine Pancreatic Secretion in Dogs

Schafmayer

Nustede²,

Köhler³

1993

Pancreas

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There have been no previous reports whether long-term bile diversion enhances pan-creatic exocrine secretion. The aim of this study was to elucidate the effect of long-term bile diversion on pancreatic exocrine secretion. Four mongrel dogs were prepared for chronic gastric and pancreatic fistulas and received intraduodenal sodium oleate infusion (controls). These dogs, then underwent diversion of bile from the intestines by ligating the common bile duct and interposing a segment of jejunum between the gallbladder and the urinary bladder (total biliary diversion [TBD]). After three weeks, the dogs received an identical sodium oleate infusion. TBD augmented basal pancreatic exocrine secretion compared with controls (4.4-fold increase in basal flow volume; 9.0-fold increase in bicarbonate output; and 3.3-fold increase in protein output). Likewise, TBD augmented oleate-stimulated exocrine secretion (2.0-fold increase in cumulative flow volume; 2.6-fold increase in bicarbonate output; and 1.4-fold increase in protein output). TBD also augmented basal and oleate-stimulated plasma cholecystokinin levels. Administration of a Cholecystokinin-A receptor antagonist (loxiglumide) after TBD reduced the flow volume and bicarbonate output to the control levels, and the protein output to less than a half of the control level. Long-term bile diversion enhances basal and oleate-stimulated pancreatic exocrine secretion, at least partly via increased cholecystokinin secretion. biliary diversion; chronic pancreatic fistula; pancreatic exocrine secretion; cholecystokinin; loxiglumide

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Gastrin-releasing peptide and CCK after intraduodenal inhibition of proteases in dogs

et al. 1994

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Pancreatic Secretion and the Release of Cholecystokinin after a Meal in Dogs with and without Exclusion of Pancreatic Juice

Cited by 7 publications

References 17 publications

Postprandial Release of Cholecystokinin after Duodenum-Preserving Total Pancreatectomy Is Independent of Intraluminal Pancreatic Protease Activity in Dogs

Postprandial Release of Cholecystokinin after Duodenum-Preserving Total Pancreatectomy Is Independent of Intraluminal Pancreatic Protease Activity in Dogs

Feedback Regulation of Exocrine Pancreatic Secretion in Dogs

Gastrin-releasing peptide and CCK after intraduodenal inhibition of proteases in dogs

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