Scientists have demonstrated the harmful effects of saturated fats on heart health, while omega-3 fatty acids like EPA show protective effects.

A recent study by a Japanese research team reveals how EPA helps maintain calcium homeostasis in heart cells disrupted by saturated fats, involving key pathways and regulatory proteins that could guide future dietary recommendations and health guidelines.

Over the past few decades, scientists have generated a pile of evidence suggesting that a diet rich in saturated fats is enough to cause heart diseases. Besides other problems like diabetes and atherosclerosis, saturated fats have also been linked to life-threatening arrhythmias. Interestingly, based on animal and human studies, certain omega-3 polyunsaturated fatty acids seem to have beneficial effects on cardiovascular health. In particular, eicosapentaenoic acid (EPA), which is found in fish oil, not only has vasodilator and antiplatelet effects, but can even help prevent atrial fibrillation and other arrythmias. Despite EPA being readily available as a dietary supplement, the effect of EPA on cardiomyocytes and their underlying mechanisms of action are not fully understood. In a recent study published online in the International Journal of Molecular Sciences, a research team from Japan set out to bridge this knowledge gap. Led by Associate Professor Masaki Morishima from Kindai University, they investigated the role of EPA in inducing long-term electrical changes in cultured mouse cardiomyocytes using a variety of bioanalytical techniques. Their research article was co-authored by Dr. Katsushige Ono from Oita University and Dr. Kazuki Horikawa from Tokushima University.

The main focus of this work was on how an oleic acid/palmitic acid mixture (OAPA), two well-studied saturated fats, impact calcium homeostasis in cardiomyocytes by affecting Ca2+ ion channels, and whether EPA can rescue these changes and restore normal functioning. First, using real-time PCR, the researchers found that OAPA markedly reduced the mRNA levels of Cav1.2 L-type Ca2+ channels. Live cell imaging systems confirmed that OAPA also lowered the spontaneous beating rate of cardiomyocytes.

Notably, these changes were prevented when even a small amount of EPA was applied together with OAPA, rescuing both mRNA and protein expression levels of Cav1.2. Through electrophysiological measurements, the researchers also confirmed that the reduction in Cav1.2 channel current caused by OAPA was also prevented by EPA.