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This Article Full Text Full Text (PDF) All Versions of this Article: 286/3/G395    most recent 00020.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Reeve, J. R. Articles by Coskun, T. Search for Related Content PubMed PubMed Citation Articles by Reeve, J. R., Jr. Articles by Coskun, T.

HORMONES AND SIGNALING

Differential bile-pancreatic secretory effects of CCK-58 and CCK-8

¹CURE Digestive Diseases Research Center, Veterans Affairs Greater Los Angeles Health Care System, Los Angeles 90073 and Digestive Diseases Division, University of California Los Angeles School of Medicine, Los Angeles 90024; ²Pasarow Mass Spectrometry Laboratory, Departments of Psychiatry and Biobehavioral Sciences and Chemistry and Biochemistry, and the Neuropsychiatric Institute, University of California, Los Angeles, California 90095; and ³Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229

Submitted 15 January 2003 ; accepted in final form 17 September 2003

In this work, we 1) synthesized rat CCK-58, 2) determined the amounts and forms of rat CCK in whole blood after stimulation of its release by casein, 3) determined the potency of CCK-8 and CCK-58 peptides to displace labeled CCK-8 from CCK_A and CCK_B receptors transfected into Chinese hamster ovary (CHO) cells, and 4) examined the biological actions of CCK-8 and rat CCK-58 in an anesthetized rat model. CCK-58 was the only detected endocrine form of CCK in rat blood. Synthetic rat CCK-58 was less potent than CCK-8 for displacing the label from CCK_A and CCK_B receptors in transfected CHO cells. However, rat CCK-58 was more potent than CCK-8 for stimulation of pancreatic protein secretion in the anesthetized rat. In addition, CCK-58 but not CCK-8 stimulated fluid secretion in this anesthetized rat model. These data suggest that regions outside the COOH terminus of rat CCK-58 influence the expression of CCK biological activity. The presence of only CCK-58 in the circulation and the fact that its biological activity differs from CCK-8 suggests that CCK-58 deserves scrutiny in other physiological models of CCK activity.

cholecystokinin

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