a Parentheses indicate an item of lesser importance. CCK, cholecystokinin; GIP, gastric inhibitory peptide.

a Parentheses indicate an item of lesser importance. CCK, cholecystokinin; GIP, gastric inhibitory peptide.

not by itself stimulate gastrin release. It allows the other stimuli to be effective.


Cholecystokinin (CCK) is structurally related to gastrin. As shown in Fig. 6 the C-terminal 5 amino acids of CCK are identical to those of gastrin. CCK was originally isolated as a 33-amino-acid peptide (Fig. 6). In addition to the 33-amino-acid form (CCK-33), CCK-39 and CCK-8 have also been isolated. The structural feature that determines whether a peptide of the gastrin-CCK family behaves like gastrin (stimulates acid secretion) or CCK (stimulates gall bladder contraction and pancreatic enzyme secretion) is the location of the tyrosyl residue. In peptides with gastrin-like activity, the tyrosyl residue is in position 6 from the C terminus, and they bind to the CCK-B receptor. Sulfation of the tyrosyl residue does not alter the potency of gastrin peptides. In CCK peptides, the tyrosyl residue is in position 7 from the C terminus, and it is always sulfated. These peptides bind to the CCK-B receptor and their pattern of activity to that of gastrin. Thus, in order to act like CCK, one of these peptides must have a sulfated tyrosyl residue in position 7 from the C terminus.

All others, including the C-terminal tetra-, penta-, and hexapeptides have gastrin-like activity. Given high enough doses, each of these two hormones can produce all the effects of the other. The difference between the two is determined by which effects occur at physiologic doses.

CCK physiologically stimulates gall bladder contraction and relaxes the sphincter of Oddi to facilitate the emptying of the gall bladder. CCK is a potent stimulator of pancreatic enzyme secretion, but only a weak stimulator of pancreatic water and bicarbonate. However, if administered with secretin, low doses of CCK greatly potentiate the secretion of bicarbonate stimulated by secretin. This important interaction is a physiologically significant effect of CCK. CCK is an important inhibitor of gastric emptying and is the reason fatty meals empty more slowly than nonfat meals. CCK also has trophic effects, stimulating the growth of the exocrine pancreas and the mucosa of the gall bladder (Table 1).

CCK is released from the I-cells of the duodenal and jejunal mucosa by peptides and single amino acids. Fatty acids or their monoglycerides containing eight or more carbon atoms are the most potent stimuli for CCK release. Fat must be in an absorbable form to release CCK; therefore, triglycerides are ineffective. Acid is a weak releaser of CCK, but may do so in high doses.

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