| Summary: | Current evidence suggests that the heart plays an important role in regulating systemic lipid homeostasis, and high-fat diet (HFD)-induced obesity is a major cause of cardiovascular disease, although little is known about the specific mechanisms involved. Exercise training can reportedly improve abnormal lipid metabolism and cardiac dysfunction induced by high-fat diets; however, the molecular mechanisms are not yet understood. In the present study, to explore the relationship between exercise training and cardiac <i>mtp</i> in HFD flies and potential mechanisms by which exercise training affects HFD flies, <i>Drosophila</i> was selected as a model organism, and the GAL4/UAS system was used to specifically knock down the target gene. Experiments revealed that HFD-fed <i>Drosophila</i> exhibited changes in body weight, increased triglycerides (TG) and dysregulated cardiac contractility, consistent with observations in mammals. Interestingly, inhibition of cardiac <i>mtp</i> expression reduced HFD-induced cardiac damage and mitigated the increase in triglycerides. Further studies showed that in HFD +<i>w<sup>1118</sup></i>, HFD + <i>Hand > w<sup>1118</sup></i>, and HFD+ <i>Hand > mtp<sup>RNAi</sup></i>, cardiac <i>mtp</i> expression downregulation induced by HFD was treated by exercise training and mitochondrial β-oxidation capacity in cardiomyocytes was reversed. Overall, knocking down <i>mtp</i> in the heart prevented an increase in systemic TG levels and protected cardiac contractility from damage caused by HFD, similar to the findings observed after exercise training. Moreover, exercise training upregulated the decrease in cardiac <i>mtp</i> expression induced by HFD. Increased Had1 and Acox3 expression were observed, consistent with changes in cardiac <i>mtp</i> expression.
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