Concanavalin A and alloxan interactions on glucose-induced insulin secretion and biosynthesis from islets of Langerhans.
The pretreatment of isolated islets of Langerhans with concanavalin A (Con A) completely blocks alloxan from suppressing the insulin release response to glucose. The lectin itself inhibits insulin secretion. This effect is dose dependent and reversible. Con A, however, has no protective action against the inhibition of glucose-induced insulin biosynthesis in islets exposed to alloxan. The protective action of Con A on alloxan toxicity is likely to be at the beta-cell surface at a membrane recognition site for glucose as a stimulus for secretion. The insulin biosynthetic effect of glucose appears to be mediated through a separate mechanism.
D000496:Alloxan / Q000494:pharmacology*; D000818:Animals; D003208:Concanavalin A / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004347:Drug Interactions; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D007328:Insulin / Q000096:biosynthesis / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D003208:Concanavalin A; D000496:Alloxan; D005947:Glucose