Cholecystokinin (CCK)-33 stimulates insulin secretion from the perfused rat pancreas: studies on the structure-activity relationship.
Cholecystokinin (CCK)-33 is known to stimulate insulin secretion. Presently, using the perfused rat pancreas, we have characterized the active site in the CCK-33 molecule that is responsible for this effect by the use of different CCK fragments. We found that CCK-33, CCK-8 and CCK-7 (1 nM) all significantly stimulated insulin secretion in the presence of 4.4 mM or 6.7 mM glucose. However, CCK-7 was much less potent than the longer forms. In contrast, CCK-4, CCK-6 and CCK-33 (1-21) had no effect on insulin secretion. We conclude that the shortest CCK-form that stimulates insulin secretion at 1 nM is the C-terminal heptapeptide CCK-7. However, CCK-8 is much more potent than CCK-7 in this respect.
D000818:Animals; D001665:Binding Sites; D002766:Cholecystokinin / Q000378:metabolism / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D010179:Pancreas / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D012844:Sincalide / Q000494:pharmacology; D013329:Structure-Activity Relationship; D013758:Tetragastrin / Q000494:pharmacology; D013997:Time Factors
D007328:Insulin; D010446:Peptide Fragments; D013758:Tetragastrin; C025997:cholecystokinin (27-33); C049129:cholecystokinin hexapeptide; D002766:Cholecystokinin; D012844:Sincalide