Abstract

Apolipoprotein B plays an essential role in systemic lipid metabolism, and it is closely related to cardiovascular diseases. Exercise-training can regulate systemic lipid metabolism, improve heart function, and improve exercise capacity, but the molecular mechanisms involved are poorly understood. We used a Drosophila model to demonstrate that exercise-training regulates the expression of apoLpp (a homolog of apolipoprotein B) in cardiomyocytes, thereby resisting heart insufficiency and low exercise capacity caused by obesity. The apoLpp is an essential lipid carrier produced in the heart and fat body of Drosophila. In a Drosophila genetic screen, low expression of apoLpp reduced obesity and cardiac dysfunction induced by a high-fat diet (HFD). Cardiac-specific inhibition indicated that reducing apoLpp in the heart during HFD reduced the triglyceride content of the whole-body and reduced heart function damage caused by HFD. In exercise-trained flies, the result was similar to the knockdown effect of apoLpp. Therefore, the inhibition of apoLpp plays an important role in HFD-induced cardiac function impairment and low exercise capacity. Although the apoLpp knockdown of cardiomyocytes alleviated damage to heart function, it did not reduce the arrhythmia and low exercise capacity caused by HFD. Exercise-training can improve this condition more effectively, and the possible reason for this difference is that exercise-training regulates climbing ability in ways to promote metabolism. Exercise-training during HFD feeding can down-regulate the expression of apoLpp, reduce the whole-body TG levels, improve cardiac recovery, and improve exercise capacity. Exercise-training can downregulate the expression of apoLpp in cardiomyocytes to resist cardiac function damage and low exercise capacity caused by HFD. The results revealed the relationship between exercise-training and apoLpp and their essential roles in regulating heart function and climbing ability.

Highlights

  • Obesity is caused by the imbalance between energy input and output and the interaction between environmental factors and susceptibility genes (Barsh et al, 2000)

  • To determine the important role of Drosophila cardiomyocytederived apoLpp in lipid metabolism, we used different degrees of knockdown to verify the differential contribution of apoLpp in the whole-body and the heart

  • The results of the Hand-Gal4 > apoLppRNAi group were similar to those of the Arm-Gal4 > apoLppRNAi group (Figure 1A). These results indicate that knockdown of apoLpp can to some extent resist the increase in high-fat diet (HFD)-induced wholebody TG levels, but it will not be like W1118 > apoLppRNAi

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Summary

Introduction

Obesity is caused by the imbalance between energy input and output and the interaction between environmental factors and susceptibility genes (Barsh et al, 2000). Obesity increases the risk of cardiovascular disease, increases blood lipids, and impairs exercise capacity (Van Gaal et al, 2006). The lipids in food (mainly triglycerides, phospholipids, and cholesterol esters) are hydrolyzed in the intestinal lumen and absorbed by the intestinal cells. The surface of CMs are covered with a monolayer of phospholipids, containing free cholesterol and apolipoprotein, which play an essential role in the transportation of triglycerides and fat-soluble vitamins. When CMs mature, they can transport lipids to the required tissues to provide energy and hydrolyze in the circulation; their products are absorbed by peripheral tissues (Hussain, 2014; Heier and Kühnlein, 2018). Exercise-training can alter the metabolic abnormalities caused by a high-fat diet (HFD). Exercise training can reduce the increase in apolipoprotein B induced by HFD (Holme et al, 2007; Rosenkilde et al, 2018)

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