title: Luminal CCK-releasing factors in the isolated vascularly perfused rat duodenojejunum.
abstract: The factors operating at the apical side of the endocrine cell releasing cholecystokinin (CCK) were investigated using the isolated vascularly perfused rat duodenojejunum. In the protease-free intestinal segment, a 30-min infusion of glucose (280 mM), oleic acid (100 mM), or triglycerides containing short- or long-chain fatty acids did not alter significantly the basal level of portal CCK-like immunoreactivity (CCK-LI), while octanoic acid (100 mM) produced a transient rise of plasma CCK-LI to approximately 250% of basal. Infusion of proteins (5% solutions of ovalbumin or casein) or of a mixture of all amino acids brought about a modest CCK secretion. In contrast, isocaloric amounts of an ovalbumin hydrolysate produced a sharp rise of portal CCK-LI to 530% of basal followed by a well-sustained plateau secretion (420% of basal) until the end of the infusion. An acid casein hydrolysate induced a slightly less pronounced CCK-LI release and was followed in decreasing order by meat, casein, and soybean peptones. Simultaneous infusion of trypsin with ovalbumin or casein hydrolysate reduced by approximately 60% the CCK release induced by peptone alone. This effect was reversed by coinfusion of soybean trypsin inhibitor (SBTI) with the trypsin-peptone mixture. Arterial infusion of tetrodotoxin (10(-6) M) or atropine (10(-5) M) had no significant effect on the trypsin-induced inhibition of peptone-mediated CCK-LI release. Administration of SBTI or camostate alone or in combination with trypsin did not alter basal CCK. Monitor peptide produced a dose-dependent transient rise of portal CCK-LI over the range from 2 to 12 micrograms.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institut National de la Santé et de la Recherche Médicale U45, Hôpital Edouard Herriot, Lyon.
authors.forename: J C
authors.initials: JC
authors.lastname: Cuber
authors.forename: G
authors.initials: G
authors.lastname: Bernard
authors.forename: T
authors.initials: T
authors.lastname: Fushiki
authors.forename: C
authors.initials: C
authors.lastname: Bernard
authors.forename: R
authors.initials: R
authors.lastname: Yamanishi
authors.forename: E
authors.initials: E
authors.lastname: Sugimoto
authors.forename: J A
authors.initials: JA
authors.lastname: Chayvialle
mesh_terms: D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002766:Cholecystokinin / Q000378:metabolism*; D004386:Duodenum / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D006133:Growth Substances; D066298:In Vitro Techniques; D036341:Intercellular Signaling Peptides and Proteins; D007583:Jejunum / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009130:Muscle, Smooth / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism; D010477:Perfusion; D011506:Proteins / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014359:Trypsin Inhibitor, Kazal Pancreatic / Q000494:pharmacology*; D014361:Trypsin Inhibitors / Q000494:pharmacology*
chemical_list: D000596:Amino Acids; D005768:Gastrointestinal Hormones; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; C504705:Spink1 protein, rat; D014361:Trypsin Inhibitors; D014359:Trypsin Inhibitor, Kazal Pancreatic; D002766:Cholecystokinin; D005947:Glucose