Effect of Intraduodenal Bile and Na-Taurodeoxycholate on Exocrine Pancreatic Secretion and on Plasma Levels of Secretin, Pancreatic Polypeptide, and Gastrin in Man
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vor 34 Jahren
The effect of intraduodenally administered cattle bile (CB) and
Na-taurodeoxycholate (TDC) on basal pancreatic secretion and plasma
levels of secretin, pancreatic polypeptide (PP), and gastrin were
investigated on two separate days in 10 fasting volunteers. Doses
of 2-6 g CB and 20&600 mg TDC were given intraduodenally at
65-min intervals. Volume, bicarbonate, lipase, trypsin, amylase,
and bilirubin were measured in 10-min fractions of duodenal juice,
and GI peptides determined by radioimmunoassay. CB and TDC enhanced
significantly and dose-dependently volume, bicarbonate and enzyme
secretion, and plasma secretin and PP levels. In contrast, plasma
gastrin showed only a marginal increase. We conclude that the
hydrokinetic effect of intraduodenal CB and TDC is at least
partially mediated by secretin. Gastrin could be ruled out as a
mediator of the ecbolic effect, whereas other GI peptides,
primarily CCK, and/or neural mechanisms must be considered possible
mediators. Both pathways may also play a role in the PP release.
Na-taurodeoxycholate (TDC) on basal pancreatic secretion and plasma
levels of secretin, pancreatic polypeptide (PP), and gastrin were
investigated on two separate days in 10 fasting volunteers. Doses
of 2-6 g CB and 20&600 mg TDC were given intraduodenally at
65-min intervals. Volume, bicarbonate, lipase, trypsin, amylase,
and bilirubin were measured in 10-min fractions of duodenal juice,
and GI peptides determined by radioimmunoassay. CB and TDC enhanced
significantly and dose-dependently volume, bicarbonate and enzyme
secretion, and plasma secretin and PP levels. In contrast, plasma
gastrin showed only a marginal increase. We conclude that the
hydrokinetic effect of intraduodenal CB and TDC is at least
partially mediated by secretin. Gastrin could be ruled out as a
mediator of the ecbolic effect, whereas other GI peptides,
primarily CCK, and/or neural mechanisms must be considered possible
mediators. Both pathways may also play a role in the PP release.
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