Inhibition of pancreatic β-cell ca2+/calmodulin-dependent protein kinase ii reduces glucose-stimulated calcium influx and insulin secretion, impairing glucose tolerance

Prasanna K. Dadi, Nicholas C. Vierra, Alessandro Ustione, David W. Piston, Roger J. Colbran, David A. Jacobson

Research output: Contribution to journalArticle

32 Scopus citations

Abstract

Background: Glucose activates CaMKII in β-cells, how this influences glucose homeostasis has not been determined. Results: Inhibiting CaMKII in mouse β-cells causes glucose intolerance by reducing Ca2+ entry and insulin secretion. Conclusion: CaMKII is a β-cell Ca2+ sensor that amplifies secretagogue-induced Ca2+ entry and insulin secretion to maintain glucose homeostasis. Significance: This provides the first evidence that β-cell CaMKII modulates glucose homeostasis under physiological and insulin resistant states.

Original languageEnglish
Pages (from-to)12435-12445
Number of pages11
JournalJournal of Biological Chemistry
Volume289
Issue number18
DOIs
StatePublished - 2014

Fingerprint Dive into the research topics of 'Inhibition of pancreatic β-cell ca2+/calmodulin-dependent protein kinase ii reduces glucose-stimulated calcium influx and insulin secretion, impairing glucose tolerance'. Together they form a unique fingerprint.

  • Cite this