Effects of two cholecystokinin variants, CCK-39 and CCK-8, on basal and stimulated insulin secretion (original) (raw)

1981, Acta Diabetologica Latina

Gastrointestinal hormones are known to influence the secretion of insulin. The more marked insulin release induced by an oral intake of glucose compared to that obtained by i.v. administration of the same amount of glucose has been largely attributed to these hormones (see recent review)5 It has long been suggested that cholecystokinin (CCK) played a role in this gastrointestinal potentiation of insulin release 40. CCK is released by intake of a mea125 and administration of CCK has been shown to stimulate insulin release in several species 14,15,1d,21,33,35,37,3&4o,42. However, results showing no effect of CCK in this respect have also been published, suggesting that the insulin secretory effect demonstrated was caused mainly by impurities s, 13,34 CCK has been shown to occur in several different forms, and CCK variants with 39, 33, and 8 amino acids have been described 7'28. The physiological significance of these different CCK variants is still far from having been elucidated although most of the evidence available suggests that the biological activity of CCK is largely confined to the C-terminal octapeptide (CCK-8)30 In the present study the in vivo effects of two different CCK molecules on basal and stimulated insulin release were studied in the mouse. The two forms of CCK used were a pure preparation of CCK-39 27 and the carboxyherminal octapeptide, CCK-8 30. The effects of these two peptides on basal insulin secretion as well as insulin release stimulated by D-glucose, the cholinergic agonist carbachol, and the ~-adrenergic agonist L-isopropylnoradrenaline (L-IPNA) were compared. Additionally, influences of the muscarinic blocker methylatropine and the [3-adrenergic blocker L-propranolol on CCK-induced insulin secretion were investigated.