In a surprising discovery, scientists have found that the heart possesses “sweet taste” receptors, similar to those on our tongues, and that stimulating these receptors with sweet substances can modulate the heartbeat. This research opens new avenues for understanding heart function and potentially for developing novel treatments for heart failure.
While taste receptors are traditionally associated with the tongue and our ability to perceive flavors, recent studies have shown that these receptors exist in other parts of the body, where they likely play different roles. This new study is the first to identify specific “sweet taste” receptors, known as TAS1R2 and TAS1R3, on the surface of heart muscle cells. The work will be presented at the 69th Biophysical Society Annual Meeting, to be held February 15 – 19, 2025 in Los Angeles.
The new research found that these receptors are not just present on heart muscle, but also functional. When the researchers stimulated these receptors in both human and mouse heart cells using aspartame, a common artificial sweetener, they observed a significant increase in the force of heart muscle contraction and accelerated calcium handling – key processes for a healthy heartbeat.
“After you eat a meal, it’s been shown that your heart rate and blood pressure actually are increasing,” said Micah Yoder, a graduate student in the lab of Jonathan Kirk at Loyola University Chicago. “Previously, this was thought to be a neural axis that’s being signaled. But we’re proposing a more direct consequence, where we have a spike in our blood sugar after eating a meal, and that’s binding to these sweet taste receptors on the heart muscle cells, causing a difference in the heartbeat,” he added.
Intriguingly, the researchers also found that these receptors are more abundant in the hearts of patients with heart failure, suggesting a possible link to disease. Further investigation revealed that stimulating the receptors triggers a cascade of molecular events within the heart cells, involving key proteins that control calcium flow and muscle contraction.
“During heart failure, the heart is changing its energetic landscape and prioritizing glucose uptake and glucose usage. So, it’s possible that during this energetic change, the heart might need to change its nutrient sensing abilities to accommodate this switch,” Yoder explained.
Additionally, their research may explain why high consumption of artificially sweetened beverages is linked to arrhythmogenesis, or an irregular heartbeat. Not only are these sweet taste receptors particularly stimulated by artificial sweeteners like aspartame, Yoder noted, he found that overstimulation of these sweet taste receptors lead to a an increase in arrhythmic like behavior in the heart cells.
But further research is needed to fully understand the long-term effects of stimulating these receptors in the heart as well as how these receptors might be targeted to strengthen the heart in the case of heart failure.
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