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CaV2.3 calcium channels control second-phase insulin release

Xingjun Jing1, Dai-Qing Li, Charlotta S Olofsson

  • 1Diabetes Programme at Lund University, Lund, Sweden.

The Journal of Clinical Investigation
|January 5, 2005
PubMed

Insights

R-type calcium channels (CaV2.3) are crucial for sustained insulin release from pancreatic islets. Ablation of CaV2.3 channels impairs second-phase insulin secretion and affects islet cell differentiation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Physiology

Background:

  • Insulin secretion kinetics are influenced by various voltage-gated calcium channel isoforms.
  • The specific contribution of R-type Ca(V)2.3 channels to this process requires elucidation.

Purpose of the Study:

  • To investigate the role of R-type Ca(V)2.3 channels in glucose-evoked insulin secretion from pancreatic islets.
  • To determine the impact of Ca(V)2.3 channel function on both first- and second-phase insulin release.

Main Methods:

  • Utilized Ca(V)2.3-knockout (Ca(V)2.3(-/-)) mouse models and pharmacological blockade with SNX482.
  • Performed dynamic insulin-release measurements and oscillatory calcium signaling analysis in pancreatic islets.
  • Assessed granule recruitment and glucagon secretion in wild-type and Ca(V)2.3(-/-) islets.

Main Results:

  • Ca(V)2.3(-/-) islets showed a 20% reduction in glucose-evoked insulin secretion, primarily affecting second-phase release.
  • Genetic or pharmacological Ca(V)2.3 ablation suppressed oscillatory calcium signaling by 18% and granule replenishment by 25%.
  • Impaired glucose-mediated suppression of glucagon secretion was observed in Ca(V)2.3(-/-) islets.

Conclusions:

  • R-type Ca(V)2.3 channels play a specific role in mediating second-phase insulin release by facilitating calcium entry for granule pool replenishment.
  • Ca(V)2.3 channels are implicated in islet cell differentiation, potentially influencing insulin and glucagon co-expression.

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