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• W2889865092 abstract "All animals inhabit environments where resource availabilitys fluctuates, making periods of fasting and starvation a ubiquitous ecological challenge. During starvation, animals can minimize energetic demands by reducing metabolic rate, body mass, body temperature and organ size. However, such wholesale metabolic suppression can compromise aerobic capacity and thus the ability to perform critical activities such as predator escape, foraging and refeeding when food becomes available (Wang, Young, & Randall, 2006). Changes to mitochondrial content and function also commonly accompany prolonged starvation in multiple taxa (e.g., Monternier, Marmillot, Rouanet, & Roussel, 2014; Staples & Brown, 2008; Trzcionka, Withers, Klingenspor, & Jastroch, 2008). However, it has been difficult for researchers to determine the benefits and costs of mitochondrial modifications in living organisms due to technological limitations. A recent study by Salin et al. (2018) represents a major advancement in the field, as they applied a novel technique to quantify in vivo reactive oxygen species (ROS) production and determined whether starvation-induced changes in mitochondrial function come at the cost of oxidative stress. Mitochondria produce energy in the form of adenosine triphosphate (ATP), via a mechanism that can be compared to a system of mechanical gears. ATP production is coupled to oxygen consumption through an electrochemical gradient of protons, the proton motive force (Figure 1). A large proton motive force provides a strong driving force for metabolism, but if it becomes too high can lead to excess ROS production (Korshunov, Skulachev, & Starkov, 1997; Munro & Treberg, 2017). Proton leak acts as a safety valve that mitigates ROS production by dissipating the proton motive force, preventing it from climbing too high. Thus, mitochondrial uncoupling reduces oxidative damage accumulation and increases longevity (Caldeira da Silva, Cerqueira, Barbosa, Medeiros, & Kowaltowski, 2008; Salin, Luquet, Rey, Roussel, & Voituron, 2012; Speakman et al., 2004). However, proton leak dissipates energy as heat, reducing potential ATP production per nutrient catabolized and contributing to increases in basal metabolic rates (Rolfe & Brand, 1996). When resources are limited, reducing proton leak to couple mitochondria will lower energetic demands, maximize the amount of ATP produced per nutrient consumed and preserve mitochondrial ATP production capacity, to enhance starvation tolerance (Monternier et al., 2014, 2017 ; Roussel, Boël, & Romestaing, 2018). As a result, Salin and colleagues hypothesized that the benefits of mitochondrial coupling during starvation are offset by the cost of increased reactive oxygen species (ROS) generation. Salin et al. (2018) exposed brown trout (Salmo trutta) to an ecologically relevant starvation challenge and used a ratiometric probe (MitoB) to measure in vivo ROS production, combined with high-resolution respirometry to characterize mitochondrial function in vitro. Food-deprived trout reduced their energy demands by decreasing liver size and mitochondrial content. At the same time, liver mitochondrial coupling was enhanced by a coordinated reduction in leak, increased oxidative phosphorylation capacity and larger proton motive force. Thus, starving trout shift gears to simultaneously reduce energetic demands and maximize energy production (Salin et al., 2018). This may explain how these trout can maintain their aerobic scope during starvation (Auer, Salin, Rudolf, Anderson, & Metcalfe, 2016), facilitating continued growth, locomotion and feeding capacity during food shortages (Auer, Salin, Anderson, & Metcalfe, 2015; Auer, Salin, Rudolf, Anderson, & Metcalfe, 2015; Auer, Salin, Rudolf, Anderson, & Metcalfe, 2015). Starved individuals, however, also produced twice as much ROS compared to fed fish, potentially due to the higher proton motive force (Salin et al., 2018). If the increase in ROS is not countered by a sufficient upregulation in antioxidant defences, oxidative stress may result, and indeed, prior work has shown that brown trout accumulate oxidative damage during prolonged starvation (Bayir et al., 2011). If not repaired, oxidative damage leads to accelerated ageing and reduced longevity (Finkel & Holbrook, 2000). Thus, oxidative stress can elicit life-history trade-offs between survival, growth and reproduction, constraining life-history evolution (Dowling & Simmons, 2009). An exciting area for future research will be to determine the long-term consequences of changes in mitochondrial coupling for organismal performance and fitness. An important implication of the findings by Salin et al. (2018) is that adaptive responses to starvation are context dependent, wherein the appropriate strategy for responding to limitations in energy supply will be determined by the energy demand, set by ecological factors and life history. For many animals, starvation coincides with periods of intermittently high energetic demands, such as the need to actively search for food, evade predators or care for young. In these cases, increased mitochondrial coupling may be worth the price to avoid an extreme imbalance between energy supply and demand. Otherwise, if imbalances between energy supply and demand can be avoided, for example by severely curtailing activity or increasing nutrient storage, then reducing proton leak may not be a desirable strategy. This is consistent with the finding that mitochondria isolated from hibernators exhibit suppressed rates of ATP production and no change in proton leak. Uncoupling may also be favoured when proton leak provides an important heat source (Staples & Brown, 2008). Comparative studies in a broader range of taxa are necessary to understand how complex ecological contexts shape metabolic responses to resource limitations. The work by Salin and colleagues in brown trout provides compelling evidence that the benefits of mitochondrial coupling for preserving organismal metabolic capacity during starvation may be offset by the cost of oxidative stress (Salin et al., 2018). To test the hypothesis that sensitivity to oxidative stress contributes to determining the best metabolic strategy to use during starvation, researchers could simultaneously manipulate food supply and energy demand (e.g., manipulating activity or immune activation) in organisms that vary in susceptibility to oxidative stress. In addition, tissue-specific mitochondrial modifications have emergent properties that shape whole organismal metabolism (Rolfe & Brand, 1996; Salin et al., 2016). Consistent with this, the results of this study illustrate how changes in mitochondrial function can synergize with changes in organ size to better balance energy supply and demand. Moving forward, integrative studies that apply technological innovations in ecologically relevant contexts are required to shed new light on the role of energetics in organismal evolutionary history, as exemplified by Salin et al. (2018). We would like to thank Andre Szejner Sigal, Kaitlin Allen and Charles Fox for their thoughtful comments and feedback on this commentary." @default.
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• W2889865092 date "2018-09-01" @default.
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• W2889865092 title "Costs of being hungry in a fast‐paced world" @default.
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• W2889865092 doi "https://doi.org/10.1111/1365-2435.13187" @default.
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