The insulinotropic action of nutrients is coupled to their catabolism in pan creatic islet b cells. CO₂ generated by the oxidation of nutrient secretagogues was recently proposed to leave b cells mainly as HCO₃^-. As a mechanism for HCO₃^-membrane transport, we searched for possible expression of NBCe1-A in b cells, an electrogenic cotransporterwhich mediates in the renal proximal tubule the exit of 1 Na⁺ together with 3 HCO₃^-and, if functioning likewise in the endocrine pancreas, should depolarize the b cell.Experiments were conducted on both isolated rat islet cells and the BRIN BD11 cell line. NBCe1-A expression was demonstrated by three independent methods: immunocytochemistry, western blotting and RT-PCR. The functionality of this cotransporter was investigated by exposing islet cells to tenidap (0.1 mM), an inhibitor of this cotransport mechanism in renal proximal tubule cells. Tenidap significantly increased the net uptake of ²²Na⁺ by dispersed islet cells, a finding compatible with the coupling of Na⁺ and HCO₃^- exit by NBCe1-A. Tenidap also drastically inhibited glucose-stimulated insulin secretion by isolated islets.

In conclusion, the present data demonstrate the expression of NBCe1-A in b cells and support the hypothesis that an electrogenic mechanism for HCO₃^- exit may contribute to the b cell membrane depolarisation in the process of nutrient-stimulated insulin release.