par Malaisse, Willy 
;Malaisse Lagae, Francine ;Sener, Abdullah
Référence IRCS Medical Science, 11, page (280)
Publication Publié, 1983
;Malaisse Lagae, Francine ;Sener, Abdullah Référence IRCS Medical Science, 11, page (280)
Publication Publié, 1983
Article révisé par les pairs
| Résumé : | It is currently thought that the capacity of glucose to act as an insulin secretagogue greatly depends on the metabolic changes evoked by the sugar in pancreatic islet cells. Nevertheless, it was recently claimed that 2,6-dideoxy-D-allose (digitoxose) inhibits glucose-induced insulin release without affecting glucose oxidation in pancreatic islets. In the present study, we indeed observed that digitoxose (20 and 40 mM) does not significantly affect the oxidation of D-[U-14C]glucose (11.1 mM). However, digitoxose (20 and 40 mM) also failed to significantly affect insulin release evoked by D-glucose (5.6, 8.3, 11.1 and 16.7 mM) over 90 min incubation of rat pancreatic islets. At most, there was a modest trend towards inhibition of insulin release by digitoxose, not exceeding 10%. Such a trend was also observed when insulin release was stimulated, in the absence of glucose, by either 2-ketoisocaproate (10 mM) or the combination of L-leucine and L-glutamine (10 mM each). It is concluded that digitoxose does not appear to be a suitable tool to dissociate the metabolism of glucose in pancreatic islets from their secretory response to this sugar. |
