TY - JOUR
T1 - Time course of the response of myofibrillar and sarcoplasmic protein metabolism to unweighting of the soleus muscle
AU - Munoz, Kathryn A.
AU - Satarug, Soisungwan
AU - Tischler, Marc E.
N1 - Funding Information:
From the Department of Biochemisty, lJnh,ersi!v ofArizona Health Sciences Center, and Graduate Program in Nutritional Sciences, Tucson, AZ. Submitted May 29. 1992; accepted October l43 1992. Supported in part by Grant No. NAG2-384 jkom the National Aeronautics and Space Administration (NASA). Portions of this studv were conducted during the tenure of a NASA Graduate Researchers Program Fellowship to Kathvn A. Munoz. Present address: S.S., Department of Biochemistry. Faculty of Medicine, Khon-Kaen University, Thailand. Address reprint requests to Marc E. Tischler, PhD, Department of Biochemistry, Universityo f Arizona. Tucson, AZ 85724. Copyright 0 I993 by W B. Saunders Company 0026049519314208-0014$03.00J0
PY - 1993/8
Y1 - 1993/8
N2 - Contributions of altered in vivo protein synthesis and degradation to unweighting atrophy of the soleus muscle in tail-suspended young female rats were analyzed daily for up to 6 days. Specific changes in myofibrillar and sarcoplasmic proteins were also evaluated to assess their contributions to the loss of total protein. Synthesis of myofibrillar and sarcoplasmic proteins was estimated by intramuscular (IM) injection and total protein by intraperitoneal (IP) injection of flooding doses of 3H-phenylalanine. Total protein loss was greatest during the first 3 days following suspension and was a consequence of the loss of myofibrillar rather than sarcoplasmic proteins. However, synthesis of total myofibrillar and sarcoplasmic proteins diminished in parallel beginning in the first 24 hours. Therefore sarcoplasmic proteins must be spared due to a decrease in their degradation. In contrast, myofibrillar protein degradation increased, thus explaining the elevated degradation of the total pool. Following 72 hours of suspension, protein synthesis remained low, but the rate of myofibrillar protein loss diminished, suggesting a slowing of degradation. These various results show (1) acute loss of protein during unweighting atrophy is a consequence of decreased synthesis and increased degradation of myofibrillar proteins, and (2) sarcoplasmic proteins are spared due to slower degradation, likely explaining the sparing of plasma membrane receptors. Based on other published data, we propose that the slowing of atrophy after the initial response may be attributed to an increased effect of insulin.
AB - Contributions of altered in vivo protein synthesis and degradation to unweighting atrophy of the soleus muscle in tail-suspended young female rats were analyzed daily for up to 6 days. Specific changes in myofibrillar and sarcoplasmic proteins were also evaluated to assess their contributions to the loss of total protein. Synthesis of myofibrillar and sarcoplasmic proteins was estimated by intramuscular (IM) injection and total protein by intraperitoneal (IP) injection of flooding doses of 3H-phenylalanine. Total protein loss was greatest during the first 3 days following suspension and was a consequence of the loss of myofibrillar rather than sarcoplasmic proteins. However, synthesis of total myofibrillar and sarcoplasmic proteins diminished in parallel beginning in the first 24 hours. Therefore sarcoplasmic proteins must be spared due to a decrease in their degradation. In contrast, myofibrillar protein degradation increased, thus explaining the elevated degradation of the total pool. Following 72 hours of suspension, protein synthesis remained low, but the rate of myofibrillar protein loss diminished, suggesting a slowing of degradation. These various results show (1) acute loss of protein during unweighting atrophy is a consequence of decreased synthesis and increased degradation of myofibrillar proteins, and (2) sarcoplasmic proteins are spared due to slower degradation, likely explaining the sparing of plasma membrane receptors. Based on other published data, we propose that the slowing of atrophy after the initial response may be attributed to an increased effect of insulin.
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U2 - 10.1016/0026-0495(93)90014-F
DO - 10.1016/0026-0495(93)90014-F
M3 - Article
C2 - 8345803
AN - SCOPUS:0027185342
SN - 0026-0495
VL - 42
SP - 1006
EP - 1012
JO - Metabolism
JF - Metabolism
IS - 8
ER -