Data from: Decreased mitochondrial metabolic requirements in fasting animals carry an oxidative cost

1. Many animals experience periods of food shortage in their natural environment. It has been hypothesised that the metabolic responses of animals to naturally-occurring periods of food deprivation may have long-term negative impacts on their subsequent life-history.
2. In particular, reductions in energy requirements in response to fasting may help preserve limited resources but potentially come at a cost of increased oxidative stress. However, little is known about this trade-off since studies of energy metabolism are generally conducted separately from those of oxidative stress.
3. Using a novel approach that combines measurements of mitochondrial function with in vivo levels of hydrogen peroxide (H2O2) in brown trout (Salmo trutta), we show here that fasting induces energy savings in a highly metabolically active organ (the liver) but at the cost of a significant increase in H2O2, an important form of reactive oxygen species (ROS).
4. After a 2-week period of fasting, brown trout reduced their whole-liver mitochondrial respiratory capacities (state 3, state 4 and cytochrome c oxidase activity), mainly due to reductions in liver size (and hence the total mitochondrial content). This was compensated for at the level of the mitochondrion, with an increase in state 3 respiration combined with a decrease in state 4 respiration, suggesting a selective increase in the capacity to produce ATP without a concomitant increase in energy dissipated through proton leakage. However, the reduction in total hepatic metabolic capacity in fasted fish was associated with an almost two-fold increase in in vivo mitochondrial H2O2 levels (as measured by the MitoB probe).
5. The resulting increase in mitochondrial ROS, and hence potential risk of oxidative damage, provides mechanistic insight into the trade-off between the short-term energetic benefits of reducing metabolism in response to fasting and the potential long-term costs to subsequent life-history traits.

1. 许多动物在自然环境中都会经历食物匮乏的阶段。已有假说提出，动物对自然发生的食物剥夺时期的代谢反应，可能会对其后续的生活史产生长期负面影响。
2. 具体而言，为应对禁食而降低能量需求或许有助于维持有限的资源储备，但这可能会以增加氧化应激为代价。然而，目前人们对这种权衡关系知之甚少，因为能量代谢研究通常与氧化应激研究分开开展。
3. 本研究结合了线粒体功能测量与褐鳟（Salmo trutta）体内过氧化氢（H₂O₂）水平检测的创新方法，结果表明，禁食会在高代谢活性器官（肝脏）中实现能量节约，但代价是活性氧（ROS）的重要形式——过氧化氢水平显著升高。
4. 经过2周禁食后，褐鳟的全肝线粒体呼吸能力（状态3、状态4呼吸及细胞色素c氧化酶活性）有所下降，这主要源于肝脏体积缩小（进而总线粒体含量减少）。在线粒体层面，这种变化得到了补偿：状态3呼吸增强，同时状态4呼吸减弱，这提示机体选择性提升了ATP生成能力，却未伴随质子渗漏导致的能量耗散增加。不过，禁食鱼类的总肝脏代谢能力下降，却伴随着体内线粒体过氧化氢（H₂O₂）水平（通过MitoB探针检测）近乎翻倍的升高。
5. 由此产生的线粒体活性氧升高，以及随之而来的氧化损伤潜在风险，为理解禁食时降低代谢的短期能量收益与后续生活史特征可能面临的长期成本之间的权衡关系提供了机制层面的见解。