Key Points

Scientists have made a remarkable discovery about the heart's unexpected ability to sense sweetness through specific taste receptors. These receptors, previously thought to exist only on the tongue, can be found on heart muscle cells and respond to artificial sweeteners like aspartame. The research suggests that these receptors might play a crucial role in heart function, potentially affecting heartbeat and muscle contraction. This groundbreaking study opens new avenues for understanding cardiac health and could lead to innovative treatments for heart-related conditions.

Key Points: Sweet Taste Receptors Discovered in Heart Muscle Cells

  • Researchers found sweet taste receptors in heart muscle cells
  • Artificial sweeteners can modulate heart muscle contraction
  • Receptors more abundant in heart failure patients
  • Potential implications for understanding cardiac function
3 min read

Heart has 'sweet taste' receptors, can sense artificial sweeteners: Study

Groundbreaking study reveals heart has sweet taste receptors that can be triggered by artificial sweeteners, potentially impacting heart function

"We're proposing a more direct consequence, where blood sugar binds to sweet taste receptors on heart muscle cells - Micah Yoder, Loyola University Chicago"

New York, Feb 16

Researchers have found that the heart possesses "sweet taste" receptors, similar to those on our tongues, and stimulating these receptors with sweet substances can modulate the heartbeat.

The discovery opens new avenues for understanding heart function and potentially for developing novel treatments for heart failure.

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.

While taste receptors are traditionally associated with the tongue and our ability to perceive flavours, 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.

"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.

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, overstimulation of these sweet taste receptors lead to a an increase in arrhythmic like behaviour in the heart cells, researchers found.

However, 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.

The work was set to be presented at the 69th Biophysical Society Annual Meeting in Los Angeles. The Biophysical Society has been established to lead development and dissemination of knowledge in biophysics.

- IANS

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