The metabolic response to trauma and sepsis involves an increased loss
of body proteins. Specific sires of changes of protein and amino acid
metabolism have been identified. In skeletal muscle, the rate of prot
eolysis is accelerated greatly. The rate of protein synthesis also may
be increased but not enough to match thr increase in degradation. Int
ramuscular glutamine concentration is decreased because of increased e
fflux and possibly decreased de novo synthesis. In the liver, the rate
of synthesis of selected proteins (i.e., albumin,; transferrin. preal
bumin, retinol-binding protein, and fibronectin ) is decreased, wherea
s acute phase protein synthesis is accelerated. Tissues characterized
by rapidly replicating cells, such as enterocytes, immune cells, granu
lation tissue, and keratinocytes, exhibit early alterations in the cas
e of decreased protein synthesis capacity. In these tissues, glutamine
use is accelerated. Increased stress hormone (cortisol and glucagon)
and cytokine secretion. as well as intracellular glutamine depletion,
are potential mediators of altered protein metabolism in trauma and se
psis. However, the relative importance of these factors has not been c
larified. Therapy of acute protein catabolism may include the use of b
iosynthetic human growth hormone. possibly in combination with insulin
-like growth factor-1, and the administration of metabolites at pharma
cologic doses. We recently studied the effects of carnitine and alanyl
-glutamine administration in severely traumatized patients. We found t
hat both carnitine and the glutamine dipeptide restrained whole-body n
itrogen loss without affecting selected indices of protein metabolism
in the skeletal muscle. (C) Elsevier Science Inc. 1997.