TY - JOUR
T1 - Metabolism of protein, amino acids, and glucose and their response to insulin in atria and cardiac myocytes of traumatized rats
AU - Tischler, Marc E.
AU - Cammisa, Helen
N1 - Funding Information:
From the Department of Biochemistry, University of Arizona Health Sciences Center, Tucson, AZ. Portions of this work were done during the tenure by M. Tischler of an Established Investigatorship of the American Heart Association and with funds from a Grant-in-Aid from the American Heart Association, Arizona Afiliate. and a grant from Merck Sharp & Dohme Research Laboratories. Address reprint requests to Dr Marc E. Tischler, Department of Biochemistry, Arizona Health Sciences Center, Tucson, AZ 85724. o I984 by Grune & Stratton, Inc. 0026-0495/84/3306~005$03.00/0
PY - 1984/6
Y1 - 1984/6
N2 - 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.
AB - 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.
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U2 - 10.1016/0026-0495(84)90005-2
DO - 10.1016/0026-0495(84)90005-2
M3 - Article
C2 - 6374367
AN - SCOPUS:0021142704
SN - 0026-0495
VL - 33
SP - 515
EP - 520
JO - Metabolism
JF - Metabolism
IS - 6
ER -