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Systemic and mitochondrial effects of metabolic inflexibility induced by high fat diet in Drosophila melanogaster
Insect Biochemistry and Molecular Biology ( IF 3.8 ) Pub Date : 2021-02-21 , DOI: 10.1016/j.ibmb.2021.103556
Robert J Cormier 1 , Rebekah Strang 1 , Hichem Menail 1 , Mohamed Touaibia 2 , Nicolas Pichaud 1
Affiliation  

Metabolic inflexibility is a condition that occurs following a nutritional stress which causes blunted fuel switching at the mitochondrial level in response to hormonal and cellular signalling. Linked to obesity and obesity related disorders, chronic exposure to a high fat diet (HFD) in animal models has been extensively used to induce metabolic inflexibility and investigate the development of various metabolic diseases. However, many questions concerning the systemic and mitochondrial responses to metabolic inflexibility remain. In this study, we investigated the global and mitochondrial variations following a 10-day exposure to a HFD in adult Drosophila melanogaster. Our results show that following 10-day exposure to the HFD, mitochondrial respiration rates measured in isolated mitochondria at the level of complex I were decreased. This was associated with increased contributions of non-classical providers of electrons to the electron transport system (ETS) such as the proline dehydrogenase (ProDH) and the mitochondrial glycerol-3-phosphate dehydrogenase (mtG3PDH) alleviating complex I dysfunctions, as well as with increased ROS production per molecule of oxygen consumed. Our results also show an accumulation of metabolites from multiple different metabolic pathways in whole adult Drosophila and a drastic shift in the lipid profile which translated into decreased proportion of saturated and monounsaturated fatty acids combined with an increased proportion of polyunsaturated fatty acids. Thus, our results demonstrate the various responses to the HFD treatment in adult Drosophila melanogaster that are hallmarks of the development of metabolic inflexibility and reinforce this organism as a suitable model for the study of metabolic disorders.



中文翻译:

黑腹果蝇高脂肪饮食诱导代谢不灵活的全身和线粒体效应

代谢不灵活是在营养应激后发生的一种情况,营养应激会导致线粒体水平的燃料转换减弱,以响应激素和细胞信号。与肥胖和肥胖相关疾病相关,在动物模型中长期暴露于高脂肪饮食 (HFD) 已被广泛用于诱导代谢不灵活和研究各种代谢疾病的发展。然而,关于代谢不灵活的全身和线粒体反应的许多问题仍然存在。在这项研究中,我们调查了成年黑腹果蝇暴露于 HFD 10 天后的整体和线粒体变化我们的结果表明,暴露于 HFD 10 天后,在复合物 I 水平的分离线粒体中测量的线粒体呼吸速率降低。这与非经典电子提供者对电子传递系统 (ETS) 的贡献增加有关,例如脯氨酸脱氢酶 (ProDH) 和线粒体 3-磷酸甘油脱氢酶 (mtG3PDH) 减轻复合物 I 功能障碍,以及每消耗一个氧分子增加 ROS 的产生。我们的结果还显示了整个成年果蝇中来自多种不同代谢途径的代谢物的积累以及脂质谱的急剧变化,这转化为饱和和单不饱和脂肪酸的比例减少,同时多不饱和脂肪酸的比例增加。因此,我们的结果证明了成年黑腹果蝇对 HFD 治疗的各种反应,这些反应是代谢不灵活发展的标志,并强化了这种生物体作为研究代谢紊乱的合适模型。

更新日期:2021-02-21
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