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Purpose Metabolic syndrome (MetS) became a tremendous public health burden in the last decades. Store-operated calcium entry (SOCE) is a unique mechanism that causes a calcium influx, which is triggered by calcium store depletion. MetS-induced alterations in cardiac calcium signaling, especially in SOCE are still unclear. Therefore, we aim to examine the possible role of SOCE and its components (STIM1 and Orai1) in the MetS-induced cardiac remodeling. Methods We used male, adult (12 weeks) Wistar albino rats (n = 20). Animals were randomly divided into two groups which were: control (C) and MetS. We gave 33% sucrose solution to animals instead of water for 24 weeks to establish MetS model. In the end, papillary muscle function was evaluated, and various electrophysiological analyses were made in isolated cardiomyocytes. Additionally, STIM1 and Orai1 protein and mRNA expressions were analyzed. Results We observed a deterioration in contractility in MetS animals and demonstrated the contribution of SOCE by applying a SOCE inhibitor (BTP2). Calcium spark frequency was increased while its amplitude was decreasing in MetS hearts, which was reversed after SOCE inhibition. The amplitude of transient calcium changes in the MetS group was decreased, and it decreased further BTP2 application. Both protein and mRNA levels of STIM1 and Orai1 were increased significantly in MetS hearts. Conclusion Current data indicate the significant contribution of SOCE to cardiac calcium handling in the MetS model. We think MetS-induced SOCE activation is a compensation mechanism that is required for the continuum of proper cardiac functioning, although the activation can also cause cardiac hypertrophy.

STIM1-Orai1 interaction mediated calcium influx activation contributes to cardiac contractility of insulin-resistant rats