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Under homeostatic conditions, Nrf2 affects the mitochondrial membrane potential, fatty acid oxidation, availability of substrates (NADH and FADH2/succinate) for respiration, and ATP synthesis.
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According to the redox mechanism for selective oxidation reactions, availability of lattice oxygen to the gaseous reactants appears to be an important parameter for activity and selectivity of oxidation catalysts.
Mitochondrial deficiencies limit the capacity of oxidative tissues to adapt fat oxidation to fat availability, leading to the accumulation of lipids in non-adipose tissues, such as skeletal muscle.
However, the phosphate ions generated during fosetyl oxidation decreased iron availability, what hampered organic matter degradation.
The experiments conducted in the galvanodynamic mode suggested that the rate limiter for hydrogen oxidation was the availability of surface hydrogen at the anode/electrolyte interface.
This phenomenon refers to the inability to adjust fuel oxidation to substrate availability.
Metabolic flexibility is the ability to adjust fuel oxidation to fuel availability.
The ability to adjust nutrient oxidation to the availability of fuels is an important mechanism for organisms to adapt to differing physiological and nutritional conditions.
The capacity of an organism, an organ, or a single cell to adapt fuel oxidation to fuel availability is termed metabolic flexibility (Galgani et al, 2008).
The rate of utilization of acetyl-CoA, the product of β-oxidation, and the availability of free fatty acids are the determining factors that control fatty acid oxidation.
Although the mechanisms underlying the intermuscle variability in HFD-induced myosteatosis are presently not defined, these findings confirm that oxidative muscles dispose free fatty acids by oxidation when their plasma availability is elevated.
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