PMID- 15583050 OWN - NLM STAT- MEDLINE DCOM- 20071016 LR - 20211203 IS - 1525-3163 (Electronic) IS - 0021-8812 (Linking) VI - 83 IP - 1 DP - 2005 Jan TI - Nutrient restriction differentially modulates the mammalian target of rapamycin signaling and the ubiquitin-proteasome system in skeletal muscle of cows and their fetuses. PG - 117-23 AB - The mammalian target of rapamycin (mTOR) signaling controls nutrient-stimulated protein synthesis in skeletal muscle, whereas ubiquitin-proteasome systems control the degradation of myofibrillar proteins. The objective of this study was to elucidate the effect of nutrient restriction on the mTOR signaling and ubiquitin-proteasome system in the skeletal muscle of cows and their fetuses. Beginning 30 d after conception, 20 cows were fed either a control diet that provided 100% nutrient requirements or a nutrient-restricted diet at 68.1% of NE(m) and 86.7% of metabolizable protein requirement. Cows were slaughtered on 125 d of gestation, and the LM of both cows and fetuses was sampled for the measurement of mTOR, ribosomal protein S6, adenosine 5'-monophosphate-activated protein kinase (AMPK), and protein ubiquitylation. When comparing the muscle samples from nutrient-restricted and control cows and their fetuses, no difference was observed for the content of mTOR and ribosomal protein S6, but the phosphorylation of mTOR at Ser(2448) and ribosomal protein S6 at Ser(235/336) were greater (P < 0.05) in control muscle than in muscle from nutrient-restricted animals. Because the phosphorylation of mTOR and ribosomal protein S6 upregulates translation, these results showed that nutrient restriction inhibits protein synthesis in muscle. The activity of AMPK in the muscle of nutrient-restricted cows was significantly lower (P = 0.05) than that of control cows. The protein ubiquitylation, however, was greater (P < 0.05) in the muscle from nutrient-restricted cows, showing accelerated protein degradation. No difference in the protein ubiquitylation was detected for fetal muscle. Data suggested that the decreased protein synthesis and promoted protein degradation resulted in muscle atrophy of pregnant cows, but not in fetal muscle. Results of this study show that in response to nutrient restriction, protein degradation was differentially regulated between cow and fetal muscle. The atrophy of cow muscle during nutrient deficiency may involve the enhanced degradation of muscle proteins. FAU - Du, M AU - Du M AD - Department of Animal Science, University of Wyoming, Laramie 82071, USA. mindu@uwyo.edu FAU - Zhu, M J AU - Zhu MJ FAU - Means, W J AU - Means WJ FAU - Hess, B W AU - Hess BW FAU - Ford, S P AU - Ford SP LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, Non-P.H.S. PL - United States TA - J Anim Sci JT - Journal of animal science JID - 8003002 RN - 0 (Antibodies) RN - 0 (Multienzyme Complexes) RN - 0 (Muscle Proteins) RN - 0 (Ribosomal Protein S6) RN - 0 (Ubiquitin) RN - EC 2.7.- (Protein Kinases) RN - EC 2.7.11.1 (Protein Serine-Threonine Kinases) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) RN - EC 2.7.11.31 (AMP-Activated Protein Kinases) RN - EC 3.4.25.1 (Proteasome Endopeptidase Complex) SB - IM MH - AMP-Activated Protein Kinases MH - *Animal Nutritional Physiological Phenomena MH - Animals MH - Antibodies/metabolism MH - Body Weight MH - Cattle/*embryology/*physiology MH - Female MH - Fetus/*physiology MH - Gene Expression Regulation, Developmental/*physiology MH - Multienzyme Complexes/analysis/metabolism MH - Muscle Proteins/metabolism MH - Muscle, Skeletal/*physiology MH - Pregnancy MH - Proteasome Endopeptidase Complex/metabolism MH - Protein Kinases/analysis/metabolism MH - Protein Serine-Threonine Kinases/analysis/metabolism MH - Ribosomal Protein S6/analysis/metabolism MH - Signal Transduction MH - TOR Serine-Threonine Kinases MH - Ubiquitin/analysis/metabolism EDAT- 2004/12/08 09:00 MHDA- 2007/10/17 09:00 CRDT- 2004/12/08 09:00 PHST- 2004/12/08 09:00 [pubmed] PHST- 2007/10/17 09:00 [medline] PHST- 2004/12/08 09:00 [entrez] AID - 83/1/117 [pii] AID - 10.2527/2005.831117x [doi] PST - ppublish SO - J Anim Sci. 2005 Jan;83(1):117-23. doi: 10.2527/2005.831117x.