Overall, these data show that semaglutide has an effect on the cardiomyocyte resulting in reduced cardiomyocyte size and cardiac mass in lean and obese mice. Because we report smaller cardiomyocytes in cultured cells and in mice treated with semaglutide, it is tempting to speculate that semaglutide may induce cardiac atrophy. However, we do not observe any changes in recognized markers of atrophy such as Murf1 and Atrogin-1. Thus, we cannot be certain that semaglutide induces atrophy per se or if it does, it may occur via molecular pathways that have not been identified herein. Of additional importance, it has been shown in previous studies that GLP1-RAs can reduce cardiac mass that was induced by persistent prohypertrophic stimuli,7,8 thus conferring benefit. However, our study shows that in the absence of prohypertrophic stressors, semaglutide causes a decrease in cardiac mass that has the potential to be detrimental in the long term. If these findings translate to humans, they may become important when considering the use of semaglutide in patients with existing CVD and associated cardiac hypertrophy vs the population of individuals using GLP1-RAs for weight loss/management, in the absence of CVD and/or the metabolic syndrome.
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