Goldfish Response to Chronic Hypoxia: Mitochondrial Respiration, Fuel Preference and Energy Metabolism.
Goldfish Response to Chronic Hypoxia: Mitochondrial Respiration, Fuel Preference and Energy Metabolism.
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DOI：
10.3390/metabo11030187
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发表时间：
2021-03-22
期刊：
影响因子：
4.1
通讯作者：
Weber JM
中科院分区：
文献类型：
--
作者：
Farhat E;Cheng H;Romestaing C;Pamenter M;Weber JM
低代谢是低氧耐受的标志性策略。为了确定代谢抑制的潜在机制，我们使用金鱼来量化慢性低氧（4周; 10%空气饱和度）对线粒体呼吸能力和燃料偏好的影响。糖酵解、β-氧化和三羧酸循环的关键酶以及Na+/K+-ATP酶的反应也在这个耐缺氧冠军的各种组织中进行了监测。结果表明，单个组织的线粒体呼吸取决于氧的可用性以及氧化的代谢燃料。本研究中测量的所有呼吸参数（LEAK、OXPHOS、呼吸控制比、CCCP-非偶联和考克斯）均受缺氧影响，至少对于其中一种代谢燃料而言。然而，除了可能有助于代谢抑制的考克斯的一般下调外，在各组织中未观察到呼吸状态变化的共同模式。缺氧导致大脑从碳水化合物转换为脂质，而其他组织没有明显的燃料偏好。它还下调脑Na+/K+-ATP酶（40%），并对糖酵解和β-氧化产生广泛的组织特异性影响。本研究表明，低氧驯化金鱼主要通过调节丙酮酸的糖酵解供应，降低脑Na+/K+-ATP酶活性，下调考克斯酶活性，降低线粒体密度，从而促进代谢抑制。
Hypometabolism is a hallmark strategy of hypoxia tolerance. To identify potential mechanisms of metabolic suppression, we have used the goldfish to quantify the effects of chronically low oxygen (4 weeks; 10% air saturation) on mitochondrial respiration capacity and fuel preference. The responses of key enzymes from glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle, and Na+/K+-ATPase were also monitored in various tissues of this champion of hypoxia tolerance. Results show that mitochondrial respiration of individual tissues depends on oxygen availability as well as metabolic fuel oxidized. All the respiration parameters measured in this study (LEAK, OXPHOS, Respiratory Control Ratio, CCCP-uncoupled, and COX) are affected by hypoxia, at least for one of the metabolic fuels. However, no common pattern of changes in respiration states is observed across tissues, except for the general downregulation of COX that may help metabolic suppression. Hypoxia causes the brain to switch from carbohydrates to lipids, with no clear fuel preference in other tissues. It also downregulates brain Na+/K+-ATPase (40%) and causes widespread tissue-specific effects on glycolysis and beta-oxidation. This study shows that hypoxia-acclimated goldfish mainly promote metabolic suppression by adjusting the glycolytic supply of pyruvate, reducing brain Na+/K+-ATPase, and downregulating COX, most likely decreasing mitochondrial density.
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影响因子：
4.5
作者：
Best, Carol;Melnyk-Lamont, Nataliya;Vijayan, Mathilakath M.
通讯作者：
Vijayan, Mathilakath M.
影响因子：
2.8
作者：
Gerber, Lucie;Clow, Kathy A.;Gamperl, Anthony K.
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Gamperl, Anthony K.
影响因子：
2.8
作者：
Bundgaard, Amanda;Qvortrup, Klaus;Fago, Angela
通讯作者：
Fago, Angela
影响因子：
2.4
作者：
MCCORMICK, SD
通讯作者：
MCCORMICK, SD
影响因子：
2.9
作者：
Kuznetsov, AV;Strobl, D;Gnaiger, E
通讯作者：
Gnaiger, E