Substrate metabolism in the metabolic response to injury

In healthy subjects the metabolic response to starvation invokes regulatory mechanisms aimed at conservation of protein mass. This response is characterized by a decrease in energy expenditure and a progressive decrease in urinary N excretion. Many non-endocrine diseases induce anorexia and a decrease in food intake. However, in contrast to the metabolic reaction to starvation in healthy subjects, anorectic patients with serious diseases have increased energy expenditure and protein catabolism, associated with profound neuroendocrine alterations. These neuroendocrine changes are induced by two mechanisms. First, afferent nerves inform the central nervous system of tissue injury which results in neuroendocrine activation. Second, tissue injury stimulates the production of inflammatory mediators, which in turn results in neuroendocrine and metabolic effects. Although these metabolic changes enable the organism to survive short-lasting diseases by using endogenous substrates, in protracted serious diseases these changes will result in loss of functioning protein mass and may endanger survival. Moreover, tissue injury alters the metabolic responses to nutrition, reflected in the persistence of catabolism as long as serious tissue injury remains.