Protein metabolism after trauma is characterized by
Injury and sepsis result in accelerated protein breakdown with increased urinary nitrogen loss and increased peripheral release of amino acids. The negative nitrogen balance represents the net result of breakdown and synthesis (with breakdown increased and synthesis increased or diminished). Amino acids such as alanine are released by muscle and transported to the liver for incorporation into acute-phase proteins including fibrinogen, complement, haptoglobin, and ferritin. The amino acids also undergo gluconeogenesis to glucose, which is utilized primarily by the brain and other glycolytic tissues such as peripheral nerves, erythrocytes, and bone marrow. Other tissues receive energy from fat in the form of fatty acids or ketone bodies during starvation following major trauma; this helps to conserve body protein. Glutamine is the most abundant amino acid in the blood, and its levels in muscle and blood decrease following injury and sepsis as it is consumed rapidly by replicating fibroblasts, lymphocytes, and intestinal endothelial cells. The use of glutamine may decrease protein catabolism in the intestine and may help prevent atrophy of the gastrointestinal tract in starved and parenterally nourished patients. Along with the counterregulatory hormones (glucagon, epinephrine, cortisol), interleukin 1 appears to mediate muscle breakdown. Recent studies have indicated that TNF (also called cachectin because of the role it plays in muscle wasting in septic or oncologic patients) also may be a principal catabolic cytokine in the traumatized patient. This protein is secreted by macrophages and further affects metabolism by inducing secretion of interleukin 1 and inhibiting synthesis and activity of lipogenic enzymes.
Decreased liver gluconeogenesis
Inhibition of skeletal muscle breakdown by interleukin 1 and tumor necrosis factor (TNF, cachectin)
Decreased urinary nitrogen loss
Hepatic synthesis of acute-phase reactants
Trauma