Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and <i>dsir</i>2 expression decline in aging <i>Drosophila</i>

// Deng-Tai Wen 1 , Lan Zheng 1 , Fan Yang 1 , Han-Zhe Li 1 and Wen-Qi Hou 1 1 Key Laboratory Of Physical Fitness and Exercise Rehabilitation of Hunan Province, Hunan Normal University, Chang Sha, 410012, Hunan Province, China Correspondence to: Lan Zheng, email: [email protected] Keywords: premature aging; high-fat-diet; exercise; dSir2; cardiac function; Gerotarget Received: November 22, 2017&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Accepted: December 08, 2017&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Published: December 15, 2017 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 dSir 2 genes are closely related to aging, but there are few directed reports showing that whether HFD could inhibit the expression dSir 2 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 dSir 2 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 dSir 2 mRNA expressions are measured. We show that endurance exercise improves climbing capacity, cardiac contraction, and dSir 2 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 dSir 2 expression decline, and prevents HFD-induced premature aging in Drosophila .