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Effect of Insulin on Glucose and Amino Acid Uptake by Skeletal Muscle Following Burn Injury. Studies with 2‐Deoxyglucose and α‐Aminoisobutyric Acid
Author(s) -
Nelson Karl M.,
Turinsky Jiri
Publication year - 1982
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 - 10.1177/014860718200600103
Subject(s) - insulin , medicine , endocrinology , basal (medicine) , glucose uptake , skeletal muscle , hindlimb , chemistry , soleus muscle , aminoisobutyric acid , amino acid , biochemistry
Basal and insulin‐stimulated uptake of 2‐deoxyglucose (2‐DG) and a‐aminoisobutyric acid (AIB) by cells of the intact soleus muscle were studied 3 days after a 3‐second scald on one hind limb of the rat. Soleus muscles from the burned and unburned limbs of burned rats, as well as from controls, were incubated with 1 mM [ 14 C]2‐DG or 50 μM [ 14 C] AIB and insulin (0, 0.1, 1.0, 10.0, or 100.0 mU/ml). Extracellular space was measured with [ 3 H]inulin. Basal uptake of 2‐DG and AIB by the cells of the burned limb muscles were 68% (p < 0.001) and 40% (p < 0.05), respectively, higher than those of controls. The intracellular concentrations of 2‐DG and AIB of burned limb muscles were 112% (p < 0.01) and 72% (p < 0.01), respectively, higher than those in control muscles. Corresponding values in soleus muscles from the unburned limb of burned rats did not differ from controls. Addition of insulin increased both the rates of cellular uptake and intracellular concentrations of 2‐DG and AIB in control and unburned limb muscles but did not significantly affect those of burned limb muscles. It is concluded that thermal injury suppresses the insulin‐induced augmentation of 2‐DG and AIB uptake by skeletal muscle underlying the burn wound but does not alter the insulin sensitivity of skeletal muscle in the unburned region. Since glucose and amino acid uptakes are stimulated by insulin independently, the cellular mechanism of the burn‐induced unresponsiveness to insulin may be located at a site which is common to both processes.