Special channels through the walls of cells in the heart control electrical impulses that regulate heart rate. Charged molecules called ions pass through these channels, generating the electrical potential needed to power the beating of the heart.
A secondary positive effect of lowering "bad" cholesterol (a type of lipid) by statins is protection of the heart from life-threatening irregular heartbeat (ventricular arrhythmia), a condition resulting from imbalances in the parasympathetic branch of the nervous system.
A new study by Jonas Gasper and his lab at Tufts-New England Medical Center, Boston, has explored the relationship between balanced lipid levels in the body and cardiac arrhythmia in chick and mouse heart cells (myocytes).
The GIRK1 ion channel is primarily responsible for electrical stimulation of myocytes during parasympathetic stimulation of the heart. Lipid-depleted chick myocytes had upregulated activity of GIRK1 and increased conductance through these ion channels.
Levels of SREBPs, proteins responsible for lipid level maintenance, were not only increased in the lipid-depleted myocytes, but SREBP-1 was also responsible for regulation of GIRK1 expression by these cells. These results were verified in a SREBP-1--deficient mouse, where GIRK1 expression was decreased compared to normal mice. Furthermore, the SREBP-1--deficient mice had hearts that were less responsive to parasympathetic stimulation, with reduced ion passage through the myocyte ion channels.
Most strikingly, following a heart attack SREBP-1--deficient mice were twice as likely to develop fast heart rates due to parasympathetic stimulation than normal mice. Taken together, these data provide a better understanding of the delicate relationship between fat metabolism and heart arrhythmia, and point the way towards new solutions for this life-threatening condition.
The artilce Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP was published in the December 3 issue of the Journal of Clinical Investigation.
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