<p>Cardiovascular diseases (CVD) are among the leading causes of mortality worldwide. Obesity and its associated metabolic disorders are recognized as major contributors to CVD risk. Recently, dietary calcium has gained attention for its potential role in preventing obesity-related metabolic disorders, though its impact on obesity-induced cardiac dysfunction remains unclear. In this study, we investigated the therapeutic effects of calcium supplementation on cardiac dysfunction in diet-induced obese rats. In this study, male Wistar rats were fed a high-fat diet for 3&#xa0;months to induce obesity. Following the development of the obese phenotype, the rats were divided into groups and fed either a low-calcium diet (0.5% Ca) or a high-calcium diet (1.0% Ca) for an additional 3&#xa0;months. At the end of the experimental period, adipose tissue, cardiac tissue, and blood samples were collected for downstream analyses, including biochemical assays, histological evaluation, enzymatic activity measurements, and protein expression studies. Our results demonstrated that increased calcium intake (1.0%) prevented obesity-induced cardiac dysfunction. Calcium supplementation reduced adiposity and restored the levels of adiponectin level. Additionally, it elevated cardiac adiponectin receptor 1, AMP-activated protein kinase (AMPK) expression, which upregulated glucose transporter 4 (GLUT4) and increased glycolytic activity. Furthermore, calcium reduced cardiac lipid accumulation, leading to decreased oxidative stress and inflammation induced by obesity. Thus, calcium supplementation during obesity improved cardiac function by increasing adiponectin mediated AMPK-mediated signaling pathway which improved cardiac glycolysis and suppressing lipid accumulation. These metabolic improvements collectively mitigated obesity-induced cardiotoxicity by suppressing oxidative stress and inflammation.</p>