Metabolism of protein, amino acids, and glucose and their response to insulin in atria and cardiac myocytes of traumatized rats.
Soft tissue injury to one hindlimb of rats was used to test the metabolic response of atrial and ventricular muscle to trauma. Effects of insulin on muscle metabolism were also studied. In myocytes and atria from normal animals, insulin increased protein synthesis and decreased protein degradation. For myocytes of rats at one and two days after trauma, this effect of insulin on proteolysis could not be detected. Over the next two days, the inhibitory effect returned to normal. Insulin also did not increase protein synthesis on day 1, but did thereafter. In atria, in contrast to heart cells, the inhibitory effect of insulin on proteolysis was enhanced at two and three days after trauma, and its stimulation of protein synthesis was unaltered. Insulin increased carbohydrate metabolism in both myocytes and atria of normal rats and traumatized rats after 2 days, and trauma did not alter this response. In myocytes, but not atria, trauma led to a faster oxidation of leucine and a significant rise in the production of alanine. Production of glutamine and glutamate was not affected in either tissue. These results show that the metabolic responses to trauma of atrial and ventricular muscle differ considerably.
D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D005947:Glucose / Q000378:metabolism*; D006325:Heart Atria / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014947:Wounds and Injuries / Q000378:metabolism*
D000596:Amino Acids; D007328:Insulin; D011506:Proteins; D005947:Glucose