Key result
Endurance exercise reverses cardiac fibrosis and dysfunction in high-fat-fed Drosophila, driven by SPARC downregulation.
Why the study?
The regulatory mechanism of endurance exercise on age-related myocardial fibrosis induced by a high-fat diet was unclear.
Does endurance exercise improve high-fat diet-induced myocardial fibrosis and cardiac dysfunction in fruit flies?
Does endurance exercise improve high-fat diet-induced myocardial fibrosis and cardiac dysfunction in fruit flies?
Endurance exercise reduces cardiac collagen deposition and prevents myocardial fibrosis and dysfunction in a Drosophila model on a high-fat diet, associated with the downregulation of SPARC.
Hypothesis-generating for SPARC-mediated exercise effects in metabolic cardiomyopathy; leaves open translation beyond Drosophila.
Myocardial fibrosis is an important pathological feature of cardiovascular aging, and a high-fat diet (HFD) can accelerate its progression, while SPARC, a remodeling-related protein, may mediate this mechanism. Endurance exercise has been shown to have cardioprotective effects, but its regulatory mechanism on age-related myocardial fibrosis induced by a high-fat diet is still unclear. This study aims to explore whether endurance exercise improves the cardiac fibrosis phenotype in high-fat-fed fruit flies by downregulating SPARC expression and elucidates its underlying molecular mechanisms. Method: Wild-type female fruit flies (n=400) within 12 hours of feathering were selected and randomly divided into four groups (n=100 per group): 10-day-old normal diet control (10D-NC), 10-day-old high-fat diet (10D-HFD), 40-day-old normal diet (40D-NC), and 10-day-old high-fat diet and exercise (10D-HE). The NC group continued to feed normal feed (including yeast, corn, and starch). The HFD group and the HE group received high-fat feed with 30% coconut oil (volume ratio) for 5 days from 5 days old. The HE group performed 2.5 hours of endurance exercise daily from 5 days of age until 10 days of age. 24 hours after the intervention, RT-qPCR was used to detect the expression level of SPARC mRNA in the heart tissue, and cardiac pulsation was recorded by an EM-CCD camera (130 frames/s). The cardiac functional parameters, such as heart rate, cardiac cycle, systolic interval, arrhythmia index, diastolic diameter, and shortening fraction, were quantified in combination with semi-automatic optical analysis software. Compared with the 10D-NC group, the expression of cardiac SPARC in the 10D-HFD group was significantly upregulated (P < 0.01), accompanied by accelerated heart rate (P < 0.001), prolonged cardiac cycle (P < 0.05), increased arrhythmia index (P < 0.001), and decreased shortening score (P < 0.001); compared with the 10D group, the expression of cardiac SPARC in the 40D group was significantly upregulated (P < 0.001), accompanied by accelerated heart rate (P < 0.001), prolonged cardiac cycle (P < 0.001), increased arrhythmia index (P < 0.05), and decreased shortening score (P < 0.05). Compared with the HFD group, SPARC expression in the HE group was significantly downregulated (P < 0.01), heart rate slowing (P < 0.001), shortening of cardiac cycle (P < 0.05), prolonging of systolic interval (P < 0.05), decreased arrhythmia index (P < 0.001), increased diastolic diameter (P < 0.05), and improved shortening score (P < 0.001). There was no statistical difference between the HE groups and the NC group in SPARC expression and various cardiac function indicators (heart rate, ejection fraction, etc.>0.05. Endurance exercise reduces the deposition of cardiac collagen and prevents myocardial fibrosis and dysfunction in Drosophila in HFD.
No takes yet. Share an insight, caveat, or question.
Huang et al. (2026) studied this question. Endurance exercise significantly downregulated SPARC expression and improved cardiac function in high-fat-fed Drosophila, reversing fibrosis and dysfunction (P < 0.01).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: