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1 CURE: Digestive Diseases Research Center, VA GLAHS, Los Angeles, CA, USA; Digestive Diseases Division, UCLA School of Medicine, Los Angeles, CA, USA
2 Pasarow Mass Spectrometry Laboratory, Departments of Psychiatry & Biobehavioral Sciences and the Neuropsychiatric Institute, and Chemistry & Biochemistry, UCLA, Los Angeles, CA, USA
3 Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
* To whom correspondence should be addressed. E-mail: jreeve{at}ucla.edu.
In this work we 1) synthesize rat CCK-58, 2) determine the amounts and forms of rat cholecystokinin in whole blood after stimulation of its release by casein, 3) determine the potency of CCK-8 and CCK-58 peptides to displace labeled CCK-8 from CCK-A and CCK-B receptors transfected into CHO cells, and 4) examine the biological actions of CCK-8 and rat CCK-58 in an anesthetized rat model. CCK-58 was the only detected endocrine form of cholecystokinin in rat blood. Synthetic rat CCK-58 was less potent that CCK-8 for displacing 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 C-terminus of rat CCK-58 influence the expression of cholecystokinin 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 cholecystokinin activity.
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  S. V. Wu, K. G. Harikumar, R. J. Burgess, J. R. Reeve Jr., and L. J. Miller Effects of cholecystokinin-58 on type 1 cholecystokinin receptor function and regulation Am J Physiol Gastrointest Liver Physiol, September 1, 2008; 295(3): G641 - G647. [Abstract] [Full Text] [PDF]
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 C. N. Sullivan, S. J. Raboin, S. Gulley, N. T. Sinzobahamvya, G. M. Green, J. R. Reeve Jr., and A. I. Sayegh Endogenous cholecystokinin reduces food intake and increases Fos-like immunoreactivity in the dorsal vagal complex but not in the myenteric plexus by CCK1 receptor in the adult rat Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1071 - R1080. [Abstract] [Full Text] [PDF]
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M. Yamamoto, J. R. Reeve Jr., D. A. Keire, and G. M. Green Water and enzyme secretion are tightly coupled in pancreatic secretion stimulated by food or CCK-58 but not by CCK-8 Am J Physiol Gastrointest Liver Physiol, May 1, 2005; 288(5): G866 - G879. [Abstract] [Full Text] [PDF]
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