Abstract
High-Fat-Diet (HFD)-induced obesity is a major contributor to heart and mobility premature aging and mortality in both Drosophila and humans. The dSir2 genes are closely related to aging, but there are few directed reports showing that whether HFD could inhibit the expression dSir2 genes. Endurance exercise can prevent fat accumulation and reverse HFD-induced cardiac dysfunction. Endurance also delays age-relate functional decline. It is unclear whether lifetime endurance exercise can combat lifetime HFD-induced heart and mobility premature aging, and relieve the harmful HFD-induced influence on the dSir2 gene and lifespan yet. In this study, flies are fed a HFD and trained from when they are 1 week old until they are 5 weeks old. Then, triacylglycerol levels, climbing index, cardiac function, lifespan, and dSir2 mRNA expressions are measured. We show that endurance exercise improves climbing capacity, cardiac contraction, and dSir2 expression, and it reduces body and heart triacylglycerol levels, heart fibrillation, and mortality in both HFD and aging flies. So, lifelong endurance exercise delays HFD-induced accelerated age-related locomotor impairment, cardiac dysfunction, death, and dSir2 expression decline, and prevents HFD-induced premature aging in Drosophila.
Highlights
HFD-induced obesity contributes to locomotor impairment, lipotoxic cardiomyopathy, and lifespan decreases in both Drosophila and humans
Lifelong endurance exercise delays HFD-induced accelerated age-related locomotor impairment, cardiac dysfunction, death, and dSir2 expression decline, and prevents HFD-induced premature aging in Drosophila
In 1-week-old flies, the relative TAG content in Normal food (NF)/E group flies was lower than normal-food control group (NF/C) group flies (LSD test, P < 0.05); the relative TAG content in high-fat-diet control group (HFD/C) group flies was higher than NF/C group flies (LSD test, P < 0.01); the relative TAG content in high-fat-diet exercise group (HFD/E) group flies was higher than HFD/C group flies (LSD test, P < 0.05), and there was no significant difference between NF/C group flies and HFD/C group flies in the relative TAG content(LSD test, P > 0.05) (Figure 1)
Summary
HFD-induced obesity contributes to locomotor impairment, lipotoxic cardiomyopathy, and lifespan decreases in both Drosophila and humans. Lipid-rich diets and obesity are associated with worldwide ‘‘epidemics’’ of cardiovascular diseases, type 2 diabetes, cancer, and locomotor impairment [2,3,4]. Reports have indicated that a lipid-rich diet is associated with obesity and a reduced lifespan in both Drosophila and humans [5,6,7]. These studies suggested that HFD-induced obesity might be a major contributor to premature aging
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