Asperlicin antagonizes stimulatory effects of cholecystokinin on isolated islets.
Asperlicin, a product derived from the fungus Aspergillus alliaceus, antagonized the multiple stimulatory effects of cholecystokinin (CCK-8S) on isolated islets. At a level of 10 microM, asperlicin completely inhibited insulin release in response to 25 nM CCK-8S. Increasing the level of CCK-8S to 100 nM partially restored a secretory response, while an even greater insulin stimulatory effect was noted with 500 nM CCK-8S. The inhibitory effect of asperlicin on CCK-8S-induced release was reversible. Asperlicin exposure had no effect on glucose or glyceraldehyde-induced secretion. Asperlicin reduced, in parallel with secretion, the increase in 3H efflux from [3H]inositol prelabeled islets usually noted with CCK-8S addition. Asperlicin did not influence the small glucose-stimulated increase in 3H efflux. The results support the notion that asperlicin is a specific and potent antagonist of the multiple stimulatory effects of CCK-8S on islet tissue.
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology*; D002766:Cholecystokinin / Q000037:antagonists & inhibitors*; D005576:Colforsin / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D005985:Glyceraldehyde / Q000494:pharmacology; D066298:In Vitro Techniques; D007294:Inositol / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects*; D008297:Male; D051381:Rats; D012636:Secretory Rate / Q000187:drug effects
D001570:Benzodiazepinones; D007328:Insulin; D005576:Colforsin; D005985:Glyceraldehyde; D007294:Inositol; D002766:Cholecystokinin; D005947:Glucose; C046367:asperlicin