Differential bile-pancreatic secretory effects of CCK-58 and CCK-8 |
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| Authors: | Reeve Joseph R Wu S Vincent Keire David A Faull Kym Chew Peter Solomon Travis E Green Gary M Coskun Tamer |
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| Affiliation: | CURE Digestive Diseases Research Center, Veterans Affairs Greater Los Angeles Healthcare System, and Digestive Diseases Division, University of California Los Angeles School of Medicine, USA. jreeve@ucla.edu |
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| Abstract: | 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. |
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