This study, based on a Drosophila model, aims to investigate the regulatory effects of endurance exercise on pect gene expression and its role in mitigating cardiac dysfunction induced by a high-sugar diet. Additionally, it seeks to determine whether endurance exercise ameliorates high-sugar-induced cardiac dysfunction and metabolic imbalance through the modulation of pect expression, thereby providing novel insights into the prevention and treatment of metabolic cardiomyopathy. A total of 300 newly eclosed virgin Drosophila melanogaster of the W1118 strain (within 12 hours of eclosion) were randomly assigned to four groups: control (NC), high-sugar sedentary (HC), normal diet with exercise (NE), and high-sugar with exercise (HE), with 100 flies per group. To generate a cardiac-specific pect knockdown line, UAS-pect virgin flies were crossed with Hand-Gal4 male flies. The high-sugar diet was formulated by supplementing a standard diet with 20% sucrose. Flies in the exercise groups underwent low-intensity endurance training on a treadmill for 2.5 hours per day, five days per week, for two consecutive weeks. After 24 hours post-intervention, pect expression levels in the heart were quantified using RT-qPCR. Cardiac function was assessed by recording 30-second heartbeat videos using an EM-CCD digital camera, and pumping function parameters were analyzed using the SOHA software. In the W1118 strain, a comparison between the NC and NE groups revealed that exercise did not significantly alter pect expression but significantly reduced heart rate (P pectRNAi knockdown strain revealed that cardiac-specific knockdown of pect led to a significant downregulation of its expression (P < 0.001), a marked reduction in heart rate (P < 0.001), and a shortened diastolic interval (P < 0.001). Conclusion: Endurance exercise modulates pect expression in response to a high-sugar diet, thereby enhancing cardiac pumping function. This study is the first to elucidate the pivotal role of pect in the crosstalk between exercise regulation and glucose-lipid metabolism, providing a molecular target for exercise-based interventions in metabolic cardiomyopathy.
Ding et al. (Thu,) studied this question.