Journal
DOMESTIC ANIMAL ENDOCRINOLOGY
Volume 57, Issue -, Pages 63-70Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.domaniend.2016.05.010
Keywords
Feed restriction; Skeletal muscle; Akt; mTOR; Lamb
Funding
- National Natural Science Foundation of China [31402053, 31472063]
- Program for the Outstanding Innovative Teams of Higher Learning Institutions of Shanxi (OIT)
- Program for the Top Young Innovative Talents of Shanxi Agricultural University [TYIT201404]
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The objective of this experiment was to investigate the mechanisms through which different levels of dietary energy affect postnatal skeletal muscle development in ewe lambs. Twelve Dorper x Small Thin-Tailed crossbred ewe Iambs (100 d of age; 20 +/- 0.5 kg BW) were selected randomly and divided into 2 groups in a completely randomized design. Animals were offered identical diets at 100% or 65% of ad libitum intake. Lambs were euthanized when BW in the ad libitum group reached 35 kg and the semitendinosus muscle was sampled. Final BW and skeletal muscle weight were decreased (P < 0.01) by feed restriction. Both muscle fiber size distribution and myofibril cross-sectional area were altered by feed restriction. Insulin-like growth factor 1 (IGF-1) messenger RNA (mRNA) content was decreased (P < 0.05) when lambs were underfed, whereas no difference for IGF-2 mRNA expression was observed (P > 0.05). Feed restriction altered phosphor-Akt protein abundance (P < 0.01). Moreover, the mammalian target of rapamycin (mTOR) pathway was inhibited by feed restriction, which was associated with decreased phosphor-mTOR, phosphorylated eukaryotic initiation factor 4E binding protein 1 (phosphor-4EBP1), and phosphorylated ribosomal protein S6 kinase (phosphor-S6K). Both mRNA expression of myostatin and its protein content were elevated in feed-restricted ewe lambs (P < 0.05). In addition, mRNA expression of both muscle RING finger 1 and muscle atrophy F-box was increased when ewe lambs were underfed. In summary, feed restriction in young growing ewe lambs attenuates skeletal muscle hypertrophy by inhibiting protein synthesis and increasing protein degradation, which may act through the Akt-dependent pathway. (C) 2016 Elsevier Inc. All rights reserved.
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