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 charact erized by a decrease in energy expenditure and a progressive decrease in ur inary N excretion. Many non-endocrine diseases induce anorexia and a decrea se in food intake. However, in contrast to the metabolic reaction to starva tion in healthy subjects, anorectic patients with serious diseases have inc reased 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 ti ssue injury which results in neuroendocrine activation. Second, tissue inju ry stimulates the production of inflammatory mediators, which in turn resul ts in neuroendocrine and metabolic effects. Although these metabolic change s enable the organism to survive short-lasting diseases by using endogenous substrates, in protracted serious diseases these changes will result in lo ss of functioning protein mass and may endanger survival. Moreover, tissue injury alters the metabolic responses to nutrition, reflected in the persis tence of catabolism as long as serious tissue injury remains.