UC Davis Health System researchers have reportedly identified “a biological pathway that is activated when blood sugar levels are abnormally high and causes irregular heartbeats, a condition known as cardiac arrhythmia that is linked with heart failure and sudden cardiac death.” Jeffrey Erickson, et al., “Diabetic hyperglycaemia activities CaMKII and arrhythmias by O-linked glycosylation,” Nature, October 2013. According to a recent press release, the study’s authors apparently found the biological link after conducting “detailed molecular experiments” using rat and human proteins and tissues, including “assessments of whole heart arrhythmias with optical mapping in isolated hearts and in live diabetic rats.”

The results evidently showed “that the moderate to high blood glucose levels characteristic of diabetes caused a sugar molecule (O-linked N-acetylglucosamine, or O-GlcNAc) in heart muscle cells to fuse to a specific site on a protein known as calcium/calmodulin dependent protein kinase II, or CaMKII.” This fusion with O-GlcNAc apparently led “to chronic overactivation of CaMKII and pathological changes in the finely tuned calcium signaling system it controls, triggering full-blown arrhythmias in just a few minutes.” The authors also reported that inhibiting CaMKII or its union with O-GlcNAc effectively prevented the arrhythmias from occurring.

“The novel molecular understanding we have uncovered paves the way for new therapeutic strategies that protect the heart health of patients with diabetes,” the senior author was quoted as saying. “Our discovery is likely to have ripple effects in many other fields. One key next step will be to deter mine if the fusion of O-GlcNAc to CaMKII contributes to neuropathies that are also common among diabetics.” See UC Davis Health System Press Release, September 29, 2013.