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Local Response of Muscle to Burns: Relationship of Glycolysis and Amino Acid Release
Author(s) -
Shangraw Robert E.,
Turinsky Jiri
Publication year - 1981
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607181005003193
Subject(s) - glutamine , medicine , hindlimb , endocrinology , metabolism , glutamate receptor , skeletal muscle , chemistry , amino acid , glycolysis , alanine , soleus muscle , carbohydrate metabolism , biochemistry , biology , receptor
The study examined the cause of, and relationship between, the increased rates of glucose utilization and amino acid release that are uniquely exhibited by skeletal muscle underlying the burn wound. Ether‐anesthetized rats were subjected to a 3‐sec one hind limb‐scald and 3 days later glucose and amino acid metabolism of soleus muscles from the burned and unburned limbs of burned rats as well as from controls was studied in vitro. Metabolism of the unburned‐limb muscle did not differ from control under any experimental conditions. In contrast, muscles from the burned limb took up to 3 times more glucose than controls in 10 mM glucose. Anoxia increased glucose uptake by all muscle groups but did not eliminate the relative enhancement exhibited by the burned‐limb muscles. Muscles from the burned limb also released 101% more alanine, 68% more glutamate, 110% more glutamine, and 163% more tyrosine in the presence or absence of medium glucose. With the exception of a uniform increase in glutamate release, anoxia did not alter amino acid releases by any muscle group. Inclusion of 1 mM iodoacetate in the glucose‐free medium reduced alanine release and raised glutamate release in all muscle groups, eliminating their relatively enhanced release by burned‐limb muscles. Iodoacetate markedly diminished glutamine release by muscles from the burned limb and caused a relatively depressed glutamine release by these muscles as compared to control. The fact that ATP‐MgCl 2 reversed the depressed release of glutamine by burned‐limb muscles suggests that cellular ATP is the limiting factor for glutamine synthesis by these muscles in iodoacetate. It is concluded that muscle hypoxia is only partially responsible for the increased glucose utilization by muscle from the burned region, and does not contribute to the augmented release of amino acids. The stimulated alanine release by muscle from the burned region does, however, appear to depend upon the increased pyruvate supply evident in these muscles.