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Kalirin/Trio Rho GDP/GTP exchange factors regulate proinsulin and insulin secretion.

Quinn Dufurrena1, Nils Bäck2, Richard E Mains3

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Summary

Kalirin and Trio proteins regulate insulin secretion by controlling Rac1 activity in pancreatic beta cells. Their loss impairs glucose-stimulated insulin release, contributing to beta-cell dysfunction.

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Molecular Signaling

Background:

  • Pancreatic beta-cell failure involves loss of glucose responsiveness and altered insulin/proinsulin ratios.
  • Secretory granule (SG) dynamics and hormone output are finely tuned by signal-mediated recruitment.
  • The GTPase Rac1 coordinates SG release, with activity regulated by Guanine nucleotide Exchange Factors (GEFs).

Purpose of the Study:

  • To investigate the roles of Kalirin and Trio, two large multidomain GEFs, in pancreatic beta-cell function.
  • To understand how Kalirin and Trio influence Rac1 activity and secretory granule exocytosis.

Main Methods:

  • Utilized small-molecule inhibitors and genetic ablation of Kalirin to manipulate GEF activity.
  • Examined age-related secretory granule behavior using radiolabeling protocols.
  • Employed a Rac1 FRET biosensor in cultured beta-cell lines to assess Rac1 localization and activity.

Main Results:

  • Loss of Kalirin/Trio function reduced proinsulin release and impaired constitutive-like secretion and exocytosis of younger granules.
  • Kalirin/Trio manipulation decreased glucose-stimulated insulin secretion.
  • Kalirin/Trio GEF1 activity was essential for glucose-induced Rac1 rearrangement to the plasma membrane.

Conclusions:

  • Kalirin and Trio are critical regulators of Rac1 activation in response to glucose metabolism.
  • These GEFs are required for normal glucose-stimulated insulin secretion, highlighting their role in beta-cell function.
  • Glucagon-like peptide-1 (GLP-1) can bypass Kalirin to restore Rac1 activity and insulin secretion, indicating Kalirin's specific role in glucose signaling pathways.