Salin 2018 Funct Ecol: Difference between revisions
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Latest revision as of 10:37, 30 August 2018
Salin K, Villasevil EM, Anderson GJ, Auer SK, Selman C, Hartley RC, Mullen W, Chinopoulos C, Metcalfe NB (2018) Decreased mitochondrial metabolic requirements in fasting animals carry an oxidative cost. Funct Ecol DOI: 10.1111/1365-2435.13125. |
ยป Open Access
Salin K, Villasevil EM, Anderson GJ, Auer SK, Selman C, Hartley RC, Mullen W, Chinopoulos C, Metcalfe NB (2018) Funct Ecol
Abstract: Many animals experience periods of food shortage in their natural environment. It has been hypothesised that the metabolic responses of animals to naturallyโoccurring periods of food deprivation may have longโterm negative impacts on their subsequent lifeโhistory.
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 tradeโoff since studies of energy metabolism are generally conducted separately from those of oxidative stress.
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).
After a 2โweek period of fasting, brown trout reduced their wholeโliver 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 twoโfold increase in in vivo mitochondrial H2O2 levels (as measured by the MitoB probe).
The resulting increase in mitochondrial ROS, and hence potential risk of oxidative damage, provides mechanistic insight into the tradeโoff between the shortโterm energetic benefits of reducing metabolism in response to fasting and the potential longโterm costs to subsequent lifeโhistory traits. โข Keywords: High-resolution respirometry, In vivo, Liver atrophy, MitoB probe, Mitochondrial respiratory state โข Bioblast editor: Kandolf G โข O2k-Network Lab: UK Glasgow Metcalfe NB, FR Plouzane Salin K
Labels: MiParea: Respiration, Comparative MiP;environmental MiP, Exercise physiology;nutrition;life style
Stress:Oxidative stress;RONS Organism: Fishes Tissue;cell: Liver Preparation: Homogenate
Coupling state: LEAK, OXPHOS
Pathway: CIV, NS, ROX
HRR: Oxygraph-2k, O2k-Fluorometer
2018-07, Safranin