A sensitive and specific bioassay for the measurement of cholecystokinin (CCK) in human plasma was developed to determine the molecular forms of CCK in circulation, CCK responses to feeding, and the physiologic role of CCK in gallbladder contraction. First, plasma was quantitatively extracted and concentrated with octadecylsilylsilica, and the extracts were then assayed for their ability to sti...

THE IDENTIFYING BIOLOGICAL actions of CCK, stimulation of gall bladder contraction (18) and pancreatic enzyme secretion (15), were first detected in extracts of small intestinal mucosa more than 75 years ago. Subsequently, the peptide responsible for these actions was isolated and characterized by Mutt and Jorpes (22). CCK is secreted by small intestinal enteroendocrine cells in response to die...

In the present study the effects of both CCK receptor agonists and antago­ nists on antinociception induced by morphine in the tail-flick test have been evalu­ ated. M orphine induced dose-dependent antinoci�eption in mice. The response of morphine was potentiated by sulfated cholecystokinin-8 (CCK-8S) but not by unsulfated cholecystokinin-8 (CCK-8U). The CCK receptor antagonists MK-329 and L-3...

BACKGROUND The peptide hormone cholecystokinin (CCK), secreted by the midgut, plays a key role in digestive physiology of vertebrates including teleosts, by stimulating pancreatic secretion, gut motility, and gallbladder contraction, as well as by delaying gastric emptying. Moreover, CCK is involved in the regulation of food intake and satiation. Secretion of CCK by the hindgut is controversial...

Expression of the brain-gut peptide cholecystokinin (CCK) in the developing olfactory-gonadotropin-releasing hormone-1 (GnRH-1) neuroendocrine systems was characterized, and the function of CCK in these systems was analyzed both in vivo and in vitro. We present novel data demonstrating that CCK transcript and protein are expressed in sensory cells in the developing olfactory epithelium and vome...

OBJECTIVE Metabolism of long-chain fatty acids within the duodenum leads to the activation of duodenal mucosal protein kinase C (PKC)-δ and the cholecystokinin (CCK)-A receptor to lower glucose production through a neuronal network. However, the interfunctional relationship between duodenal PKC-δ and CCK remains elusive. Although long-chain fatty acids activate PKC to stimulate the release of C...

In contrast to supramaximal CCK-8 or caerulein, acute or prolonged supraphysiological levels of endogenous CCK-58 do not cause pancreatitis. Compared with CCK-8, CCK-58 is a much stronger stimulant of pancreatic chloride and water secretion, equivalent to maximally effective secretin, but with a chloride-to-bicarbonate ratio characteristic of acinar fluid. Because supraphysiological endogenous ...

Cholecystokinin (CCK)-like immunoreactivity (CCK-LI) in a pool of 12 dog brains was extracted sequentially into boiling water and cold 2% trifluoroacetic acid. Gel filtration on Sephadex G-50 revealed three main molecular forms detected by a carboxyl-terminal antibody; one was eluted in the position of CCK-58 (58 amino acid residues long); a second, in the position of CCK-8; and a third, near t...

CCK(A) receptors are present on vagal afferent fibers. The objectives of this study were to identify the presence of high- and low-affinity CCK(A) receptors on nodose ganglia and to characterize the intracellular calcium signal transduction activated by CCK. Stimulation of acutely isolated nodose ganglion cells from rats with 1 nM CCK-8 primarily evoked a Ca(2+) transient followed by a sustaine...

Yamamoto M, Reeve JR, Jr, Green GM. Supramaximal CCK-58 does not induce pancreatitis in the rat: role of pancreatic water secretion. Am J Physiol Gastrointest Liver Physiol 292: G964–G974, 2007. First published January 4, 2007; doi:10.1152/ajpgi.00338.2004.—In contrast to supramaximal CCK-8 or caerulein, acute or prolonged supraphysiological levels of endogenous CCK-58 do not cause pancreatitis...