High-fat diet (HFD) induces systemic lipid metabolism disorders and cardiac dysfunction, including arrhythmias, decreased cardiac contractility, and other pathological phenotypes. Exercise as a non-pharmacological intervention has potential protective effects against metabolic diseases, but its molecular mechanisms have not been fully elucidated. Lipin genes play a pivotal role in metabolic homeostasis by integrating lipid synthesis, catabolism, and energy-sensing signals. In this study, we used Drosophila as a model to investigate whether exercise ameliorates HFD-induced cardiac dysfunction in Drosophila by regulating the expression of Lipin, a key gene for lipid metabolism. Method: Wild-type female Drosophila (n=360) within 12 hours of pinning were selected and randomly divided into three groups (n=120 per group): normal diet control (NC), high-fat diet (HFD), and high-fat exercise intervention (HE). The NC group was continuously fed a normal diet (containing yeast, corn, and starch), while the HFD and HE groups received a high-fat feed intervention containing 30% coconut oil (v/v) for 5 days starting at 5 days of age. The HE groups performed 1.5 hours of endurance exercise daily from 5 days of age until 10 days of age. Twenty-four hours after the end of the intervention, Lipin mRNA expression levels in cardiac tissues were detected by RT-qPCR, and cardiac beats were recorded by an EM-CCD camera (130 frames/s), which was combined with semiautomatic optical analysis software to quantify cardiac function parameters such as heart rate, cardiac cycle, systolic intervals, arrhythmia index, diastolic diameter, and shortening fraction. Compared with the NC group, cardiac Lipin expression was significantly upregulated in the HFD group (P 0.05), suggesting that the exercise intervention could completely reverse the HFD-induced cardiac phenotypic abnormalities. Exercise significantly ameliorates pathological phenotypes such as arrhythmia, systolic dysfunction, and reduced pumping efficiency in Drosophila on a high-fat diet by down-regulating cardiac Lipin expression.
Li et al. (Thu,) studied this question.