par Malaisse Lagae, Francine 
;Welsh, M;Lebrun, Philippe ;Herchuelz, André ;Sener, Abdullah ;Hellerström, Claes;Malaisse, Willy
Référence Diabetes (New York, N.Y.), 33, 5, page (464-469)
Publication Publié, 1984-05
;Welsh, M;Lebrun, Philippe ;Herchuelz, André ;Sener, Abdullah ;Hellerström, Claes;Malaisse, Willy Référence Diabetes (New York, N.Y.), 33, 5, page (464-469)
Publication Publié, 1984-05
Article révisé par les pairs
| Résumé : | L-Asparagine (2-10 mM) failed to affect insulin secretion from rat pancreatic islets incubated in the absence of exogenous nutrient or presence of D-glucose, but caused a dose-related and progressive enhancement of insulin release evoked by L-leucine, 2-aminobicyclo[2,2,1]heptane-2-carboxylate, or 2-ketoisocaproate. The secretory response to the combination of L-asparagine and L-leucine was augmented by theophylline and inhibited in the absence of extracellular Ca2+ or presence of either menadione or methylamine. L-Asparagine augmented leucine-stimulated 45Ca net uptake. The ATP content, rate of O2 uptake, and malate/pyruvate ratio were not significantly different in islets exposed to L-leucine alone or to both L-asparagine and L-leucine, respectively. In the sole presence of L-asparagine, however, the malate/oxalacetate ratio was decreased and the malate/pyruvate ratio increased, relative to basal values. It is proposed that the enhancing action of L-asparagine upon insulin release evoked by L-leucine might be due to an accelerated generation rate of cytosolic NADPH, rather than to any sizable increase in either islet respiration or steady-state cytosolic NADPH/NADP+ ratio. |
