semaglutide reduces the burden on the heart and promotes adaptive changes in heart health

In recent years, GLP-1 receptor agonists (such as semaglutide) have rapidly become the focus of the medical community. This type of medication not only controls appetite, but also promotes insulin secretion and enhances metabolism. Whether in the field of weight loss or prevention of cardiovascular disease, semaglutide has demonstrated its "omnipotent" characteristics.

However, some people have raised questions about the effects of semaglutide on the heart? Will it make the heart become 'weak'? Recently, the JACC: Basic to Translational Science journal published a new study showing that semaglutide can make the heart more "lightweight", reduce heart mass and myocardial cell size, but does not affect heart function and work efficiency. This is not only significant in obese mice, but also has a similar effect in thinner mice, indicating that its effect is not limited to weight loss, but also directly "shapes" the heart.

It is worth noting that although the heart mass has decreased, the heart function has not been impaired. The measurement of ejection fraction and diastolic function shows that the heart's "pumping ability" remains normal, indicating that the heart's "weight loss" is a healthy adaptive change rather than pathological atrophy.

In order to rule out the possibility of pathological changes, the research team tested the expression of genes related to fibrosis and atrophy, and no significant changes were found. This indicates that the effect of semaglutide on the heart is more like "shaping" rather than causing pathological damage.

In addition, when researchers used semaglutide on lean mice, although there was little change in body weight (only 8.2% loss of muscle mass within 3 weeks), heart mass, left ventricular mass, and myocardial cell area still significantly decreased. This result indicates that the effect of semaglutide on the heart is not solely dependent on weight loss, suggesting that its effect on the heart is direct.

Finally, in vitro experiments further confirmed through human myocardial cell culture that semaglutide can directly reduce the area of myocardial cells, indicating that its effect is not limited to weight loss or other metabolic pathways, but is achieved through direct action on the heart.

The researchers specifically pointed out that although the volume of myocardial cells decreased, no changes in biomarkers commonly associated with cardiac atrophy, such as Murf1 and Atrogin-1, were observed. Therefore, researchers are still unable to determine whether this belongs to cardiac atrophy, or whether this change may occur through an unclear mechanism.

Overall, research has shown that semaglutide not only helps with weight loss, but also effectively reduces the burden on the heart, resulting in healthy adaptive changes to the heart rather than pathological damage. This discovery provides new insights into the potential of GLP-1 receptor agonists in cardiac protection.