by Peng Xu
The pancreatic beta cell secretes insulin triggered by glucose-stimulated calcium entry. How pancreatic beta cells sense calcium entry is of great interest. Several lines of in vitro evidence suggest that calcium/calmodulin-dependent protein kinase II (CaMKII) is a key regulator of insulin secretion. However, the role of CaMKII under physiological and pathological conditions in vivo is unclear.
In a study in the Journal of Biological Chemistry, David Jacobson, Ph.D., and colleagues used a transgenic mouse model that allows conditional inhibition of beta cell CaMKII activity to investigate the physiological role of CaMKII in pancreatic beta cells. They found that inhibition of beta cell CaMKII significantly impairs glucose tolerance by reducing calcium channel activity, calcium entry and insulin secretion.
The studies reveal that CaMKII acts as a calcium sensor in a positive feedback pathway that enhances glucose-stimulated insulin secretion. Augmenting CaMKII function may represent a new target for the treatment of diabetes.
This research was supported by National Institutes of Health grants DK096122, DK081666, as well the Vanderbilt Diabetes Research and Training Center grant DK020593.
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