Abstract
Using the cold stressed, fasted animal model, a unified hypothesis is proposed to explain how the ATP “potential” of nutrients may regulate plasma corticosteroid concentration (PCC) by influencing the energy metabolism of the cells, the cellular purine release, and the pituitary-adrenal axis. The nutrient ATP potential is defined as the net number of moles of ATP generated from a mole of nutrient per number of tricarboxylic acid (TCA) cycles used for its metabolism.
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