Exercise-Training Regulates Apolipoprotein B in Drosophila to Improve HFD-Mediated Cardiac Function Damage and Low Exercise Capacity
| Autor: | Wan Li Wang, Meng Zhou, Qiu Fang Li, Meng Ding, Lan Zheng, Wan Da Peng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Cardiac function curve medicine.medical_specialty Apolipoprotein B Physiology 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Physiology (medical) Internal medicine lipid metabolism medicine apolipoprotein B QP1-981 Gene knockdown biology cardiac dysfunction business.industry food and beverages Lipid metabolism medicine.disease Obesity exercise capacity 030104 developmental biology Endocrinology biology.protein exercise-training Drosophila business Function (biology) Genetic screen |
| Zdroj: | Frontiers in Physiology, Vol 12 (2021) |
| DOI: | 10.3389/fphys.2021.650959/full |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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