Changes in food consumption patterns towards diets rich in fat and sugar have contributed to a rapid increase in overweight and obesity prevalence rates over the last few decades (National Heart and Lung and BI, 2022). As a result of globalization, these trends are not limited to the developed countries alone but apply to several developing, transition, and middle-income countries as well (Pan American Health Organization; World Health Organization, 2016; Shankar et al., 2014; Goryakin et al., 2015).

Excessive intake of sugars, especially fructose and sucrose (a dimer of glucose and fructose monomers), together with physical inactivity, are highly correlated with metabolic diseases, including obesity, diabetes, fatty liver, and cardiovascular disease (Malik and Hu, 2015; Ma et al., 2022). Cardiovascular diseases are the leading cause of death globally and are responsible for imposing huge burdens on healthcare systems and reducing the quality of life of populations around the world (Shankar et al., 2014; World Health Organization, 2021).

Diseases that affect the heart have cardiac remodeling as a common physiopathology process. Cardiac remodeling is defined as changes in gene expression resulting in molecular, cellular, and interstitial changes, which manifest clinically as changes in size, shape, and function of the heart as a result of cardiac overload or injury (Cohn et al., 2000).

Some reports show that animals fed high fructose or sucrose diets develop cardiac remodeling with changes in morphology and/or cardiac function (Arias-Chávez et al., 2022; D'Haese et al., 2023; Chung et al., 2021; Dutta et al., 2001). However, the cardiac alterations triggered by sucrose are still not well elucidated and need more attention. Matias et al. demonstrated that excess sucrose causes cardiomyocyte contractility dysfunction associated with alterations in the myocyte sensitivity to intracellular Ca2+ (Martins Matias et al., 2020). Vasanji et al. observed that hearts of Sprague-Dawley rats fed a diet of sucrose over a 10-week period displayed depressed sarcoplasmic reticulum (SR) function demonstrated by a significant reduction in SR Ca2+ uptake. The authors also observed that the decrease in SR Ca2+ uptake was associated with a significant reduction in the phosphorylation of phospholamban by both cAMP-dependent protein kinase and Ca2+/calmodulin-dependent protein kinase II (Vasanji et al., 2006). Due to this, alteration in the myocardium calcium handling seems to be an important factor involved in the cardiac dysfunction induced by high sucrose ingestion.

In the past years, there has been growing recognition that inflammation makes an important contribution to cardiac development, composition, and function (Nishida and Otsu, 2017; Swirski and Nahrendorf, 2018). However, the literature highlights that inflammation takes part in the pathophysiology of cardiac dysfunction of distinct etiologies by promoting calcium mishandling (Zhang and Dhalla, 2024; Prabhu, 2004). Thus, in this study, we used an animal model to test if sucrose-induced cardiac remodeling is related to the deterioration of myocardial contractility due to alterations in calcium-handling protein expression. In addition, we evaluated whether cardiac pro-inflammatory cytokine levels are associated with this process.