1988
DOI: 10.1111/j.1365-2362.1988.tb01173.x
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Stimulation of pancreatic secretion in man by a protease inhibitor (camostate)

Abstract: Pancreatic secretion and plasma cholecystokinin (CCK) and secretin levels were measured in 10 healthy volunteers after application of a serine protease inhibitor (camostate) to study the mechanism of feedback regulation. Camostate produced a strong inhibition of trypsin and chymotrypsin activity in duodenal juice for 1 h. This was accompanied by an increase in duodenal aspirate volume and pancreatic enzyme secretion under both basal and secretin-stimulated conditions. Due to inhibition of tryptic activity, sur… Show more

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Cited by 65 publications
(24 citation statements)
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“…This study further supports the existence of a negative feedback mechanism between plasma CCK and bile products in the lumen of the proximal small intestine (Adler et al, 1988;Gomez et al, 1988;Koop et al, 1988Koop et al, , 1989. However, other mechanisms of an augmented stimulated CCK release during loxiglumide administration, such as direct effects of loxiglumide on CCK-producing cells or indirect effects via yet to be established paracrine, neurocrine or endocrine mechanisms cannot be excluded.…”
Section: Resultsmentioning
confidence: 67%
“…This study further supports the existence of a negative feedback mechanism between plasma CCK and bile products in the lumen of the proximal small intestine (Adler et al, 1988;Gomez et al, 1988;Koop et al, 1988Koop et al, , 1989. However, other mechanisms of an augmented stimulated CCK release during loxiglumide administration, such as direct effects of loxiglumide on CCK-producing cells or indirect effects via yet to be established paracrine, neurocrine or endocrine mechanisms cannot be excluded.…”
Section: Resultsmentioning
confidence: 67%
“…Beside species differences, the use of unsuit able experimental models can be held re sponsible. In some studies trypsin inhibitors were used, which were unable to inhibit Chy motrypsin completely, and therefore unfit to study a presumably protease-specific feed back regulation [14]. The elevated plasma CCK concentrations observed in dogs after application of highly specific receptor antag onists [ 15] do not proof a role for CCK in the feedback mechanism.…”
Section: Discussionmentioning
confidence: 99%
“…This was suggested by us in 1977 [9] when we published the first evidence of the existence of such a mechanism in the human. Today most authors agree that there is a negative feedback mechanism in humans [10][11][12][13][14][15][16][17][18][19]. Although the association to the pain-relieving effect of oral enzyme therapy is not fully established, the hypothesis is that the low trypsin activity in the duodenum in patients with chronic pancreatitis induces an increase in the concen tration of circulating CCK.…”
Section: Oral Pancreatic Enzyme Therapymentioning
confidence: 99%