Effect of carbohydrates upon insulin secretion in Bufo arenarum (Amphibia:Bufonidae).

Pancreas pieces of Bufo arenarum were incubated with several sugars at basal and stimulatory concentrations, and with inhibitors of their metabolism, measuring the insulin released by radioimmunoassay. Glucose, mannose, fructose, glyceraldehyde and dihydroxyacetone all at 8 mM, significantly enhanced the release of insulin elicited by basal concentrations of these carbohydrates (2 mM). The nonmetabolizable sugars galactose and 2-deoxyglucose failed to enhance insulin secretion. N-Acetyl-glucosamine at 8 mM did not significantly affect the release of insulin. D-Glucose, but not L-glucose, at 8 mM stimulated insulin secretion above baseline (2 mM glucose). At 8 mM, the D-glucose alpha-anomer significantly increased insulin release, while this effect was not observed using the beta-anomer. Insulin release elicited by 2 mM of the alpha-anomer was significantly higher than that triggered by the beta-anomer. Iodoacetate (5 mM), and dinitrophenol (0.3 mM) exerted an inhibitory effect upon glucose-induced insulin secretion. The effect of these carbohydrates and metabolic inhibitors--tested for the first time in amphibians--was similar to that described in the mammalian pancreas, thus suggesting that such compounds play an important role in the metabolic control of insulin secretion in amphibians.

Effect of activators and inhibitors of K+ channels on insulin secretion in the amphibian pancreas.

The aim of this study was to obtain pharmacological evidence for the presence and participation of K+ channels in amphibian pancreatic islets. Pancreases from the toad Bufo arenarum were thus incubated with activators or blockers of K+ channels and the immunoreactive insulin released into the medium was measured by radioimmunoassay. Two K(+)-ATP channel openers (diazoxide and BPDZ44) inhibited; while a K(+)-ATP channel blocker (tolbutamide) and metabolizable sugars (glucose, glyceraldehyde) significantly stimulated the output of insulin. Although a nonmetabolizable sugar (galactose) failed to increase insulin release, dinitrophenol decreased the secretagogue effect of glucose. By contrast, although somatostatin and clonidine blocked the release of insulin, tetraethylammonium significantly stimulated secretion. For each compound tested, the effects on both insulin secretion and B-cell K+ channel activity were similar to those observed in the mammalian pancreas. These findings point to the existence of mammalian-like K+ channels in the B-cells of some amphibians.