Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Removal of Ca2+ channel beta3 subunit enhances Ca2+ oscillation frequency and insulin exocytosis.

An oscillatory increase in pancreatic beta cell cytoplasmic free Ca2+ concentration, [Ca2+]i, is a key feature in glucose-induced insulin release. The role of the voltage-gated Ca2+ channel beta3 subunit in the molecular regulation of these [Ca2+]i oscillations has now been clarified by using beta3 subunit-deficient beta cells. beta3 knockout mice showed a more efficient glucose homeostasis compared to wild-type mice due to increased glucose-stimulated insulin secretion. This resulted from an increased glucose-induced [Ca2+]i oscillation frequency in beta cells lacking the beta3 subunit, an effect accounted for by enhanced formation of inositol 1,4,5-trisphosphate (InsP3) and increased Ca2+ mobilization from intracellular stores. Hence, the beta3 subunit negatively modulated InsP3-induced Ca2+ release, which is not paralleled by any effect on the voltage-gated L type Ca2+ channel. Since the increase in insulin release was manifested only at high glucose concentrations, blocking the beta3 subunit in the beta cell may constitute the basis for a novel diabetes therapy.[1]

References

Removal of Ca2+ channel beta3 subunit enhances Ca2+ oscillation frequency and insulin exocytosis. Berggren, P.O., Yang, S.N., Murakami, M., Efanov, A.M., Uhles, S., Köhler, M., Moede, T., Fernström, A., Appelskog, I.B., Aspinwall, C.A., Zaitsev, S.V., Larsson, O., de Vargas, L.M., Fecher-Trost, C., Weissgerber, P., Ludwig, A., Leibiger, B., Juntti-Berggren, L., Barker, C.J., Gromada, J., Freichel, M., Leibiger, I.B., Flockerzi, V. Cell (2004) [Pubmed]

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