In pancreatic beta cells, not only insulin exocytosis per se, but translocation of beta granules toward the plasma membrane--an event upstream of exocytosis--are under the control of glucose. However, the molecular basis of this translocation has been poorly understood. Rab27a-mediated translocation of glucose-induced beta granules is reported in this issue of the JCI. Rab27a or its effector molecule may constitute a novel pharmacological target because potentiation of the Rab27a pathway is expected to restore beta cell glucose competency in patients with diabetes mellitus.
No takes yet. Share an insight, caveat, or question.
Aizawa et al. (2005) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: