|
|
||||||||
AJP - Gastrointestinal and Liver Physiology, Vol 259, Issue 2 191-G197, Copyright © 1990 by American Physiological Society
ARTICLES |
J. C. Cuber, G. Bernard, T. Fushiki, C. Bernard, R. Yamanishi, E. Sugimoto and J. A. Chayvialle
Institut National de la Sante et de la Recherche Medicale U45, Hopital Edouard Herriot, Lyon.
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)
This article has been cited by other articles:
![]() |
S. Choi, M. Lee, A. L. Shiu, S. J. Yo, G. Hallden, and G. W. Aponte GPR93 activation by protein hydrolysate induces CCK transcription and secretion in STC-1 cells Am J Physiol Gastrointest Liver Physiol, May 1, 2007; 292(5): G1366 - G1375. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Choi, M. Lee, A. L. Shiu, S. J. Yo, and G. W. Aponte Identification of a protein hydrolysate responsive G protein-coupled receptor in enterocytes Am J Physiol Gastrointest Liver Physiol, January 1, 2007; 292(1): G98 - G112. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-C. Gevrey, M. Cordier-Bussat, E. Nemoz-Gaillard, J.-A. Chayvialle, and J. Abello Co-requirement of Cyclic AMP- and Calcium-dependent Protein Kinases for Transcriptional Activation of Cholecystokinin Gene by Protein Hydrolysates J. Biol. Chem., June 14, 2002; 277(25): 22407 - 22413. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Wang, V. Prpic, G. M. Green, J. R. Reeve Jr., and R. A. Liddle Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells Am J Physiol Gastrointest Liver Physiol, January 1, 2002; 282(1): G16 - G22. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Nishi, H. Hara, T. Hira, and F. Tomita Dietary Protein Peptic Hydrolysates Stimulate Cholecystokinin Release via Direct Sensing by Rat Intestinal Mucosal Cells Experimental Biology and Medicine, December 1, 2001; 226(11): 1031 - 1036. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Juanola, M. Giralt, M. Jimenez, M. Mourelle, and P. Vergara Mucosal mast cells are involved in CCK disruption of MMC in the rat intestine Am J Physiol Gastrointest Liver Physiol, July 1, 1998; 275(1): G63 - G67. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |