Fish growth in response to different feeding regimes and the related molecular mechanism on the changes in skeletal muscle growth in grass carp (Ctenopharyngodon idellus)

Abstract Approximately 90% of beef cattle on feed in the United States receive an anabolic implant during production, which results in increased growth, efficiency, and economic return to producers. However, the molecular mechanism through which these anabolic implants operate to improve skeletal muscle growth remains unknown. The objective of this study was to determine the molecular mechanism through which estradiol (E2) and trenbolone acetate (TBA) improve skeletal muscle growth in beef cattle and to specifically understand whether E2 and/or TBA function by modulating transcription. To address this, bovine satellite cells (BSC) were isolated from three different backgrounded steers and grown in culture. Once cultures reached 75% confluency they were treated with 1% fetal bovine serum (FBS) and 10 nM E2 or 10 nM TBA. In an additional experiment, all previously listed treatments were given in addition to actinomycin D (AD, a non-specific inhibitor of transcription). Treatment with E2 or TBA increased proliferation (P < 0.05) when compared to a 1% FBS control. Furthermore, treatment with E2 or TBA in the presence of AD increased proliferation (P < 0.01) when compared to cultures treated with just AD. These results indicate that TBA and E2 are both capable of increasing proliferation of BSC cultures through non-transcriptional mechanisms. Future work will identify the TBA and E2 signaling pathways that affect muscle growth and don’t involve changes in gene transcription.

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Regulation of Protein Synthesis and Skeletal Muscle Growth

Journal of Animal Science ◽

10.2527/jas1974.3851054x ◽

1974 ◽

Vol 38 (5) ◽

pp. 1054-1070 ◽

Cited By ~ 19

Author(s):

Vernon R. Young

Keyword(s):

Skeletal Muscle ◽

Protein Synthesis ◽

Muscle Growth ◽

Skeletal Muscle Growth

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PSIX-29 JAK2-STAT3 Pathway Mediated Satellite Cell Apoptosis to Govern Skeletal Muscle Growth with Lysine

Journal of Animal Science ◽

10.1093/jas/skaa278.594 ◽

2020 ◽

Vol 98 (Supplement_4) ◽

pp. 334-334

Author(s):

Zhi-wen Song ◽

Cheng-long Jin ◽

Mao Ye ◽

Chun-qi Gao ◽

Hui-chao Yan ◽

...

Keyword(s):

Skeletal Muscle ◽

Muscle Growth ◽

Longissimus Dorsi ◽

Control Group ◽

Stat3 Pathway ◽

Skeletal Muscle Growth ◽

Longissimus Dorsi Muscle ◽

Dorsi Muscle ◽

Pathway Inhibition ◽

Induced Apoptosis

Abstract Apoptosis is programmed cell death that can be stimulated by external stress or nutrition restrictions. Lysine (Lys) is an essential amino acid for pig growth, and the relationship between Lys deficiency caused apoptosis and inhibition of skeletal muscle growth remains unknown. The objective of this study was to investigate whether apoptosis could be regulated by Lys supplementation and the potential mechanism. In current work, 30 male Duroc × Landrace × Large weaned piglets were divided randomly into 3 groups: control group (Lys 1.30%), Lys deficiency group (Lys 0.86%), and Lys rescue group (Lys 0.86%, 0-14d; 1.30%,15–28 d). The experiment lasted for 28 days, and on the morning of 29 d, piglets were slaughtered to collect samples. Isobaric tag for relative and absolute quantification (iTRAQ) proteomics analysis of the longissimus dorsi muscle showed that Janus family tyrosine kinase (JAK)-signal transducer and activator of transcription (STAT) pathway was involved in Lys deficiency-induced apoptosis and inhibited skeletal muscle growth. Meanwhile, western blotting results of the longissimus dorsi muscle demonstrated that Lys deficiency caused apoptosis (P < 0.05) with the JAK2-STAT3 pathway inhibition (P < 0.05). Interestingly, apoptosis was suppressed (P < 0.05), and the JAK2-STAT3 pathway was reactivated (P < 0.05) after Lys re-supplementation in longissimus dorsi muscle. In addition, results of satellite cells (SCs) isolated from the longissimus dorsi muscle of 5-day-old Landrace piglets showed that Lys deficiency-induced apoptosis (P < 0.05) was mediated by the JAK2-STAT3 pathway inhibition (P < 0.05). Moreover, the JAK2-STAT3 pathway was reactivated (P < 0.05) by Lys re-supplementation and suppressed apoptosis in SCs (P < 0.05), and this effect was blocked (P < 0.05) after SCs treated with AG-490 (a specific inhibitor of JAK2). Collectively, Lys inhibited apoptosis in SCs to govern skeletal muscle growth via the JAK2-STAT3 pathway.

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Why exercise builds muscles: Titin mechanosensing controls skeletal muscle growth under load

Biophysical Journal ◽

10.1016/j.bpj.2021.07.023 ◽

2021 ◽

Author(s):

Neil Ibata ◽

Eugene M. Terentjev

Keyword(s):

Skeletal Muscle ◽

Muscle Growth ◽

Skeletal Muscle Growth

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Skeletal Muscle Growth, Enzyme Activities, and the Development of Thermogenesis: A Comparison between Altricial and Precocial Birds

Physiological Zoology ◽

10.1086/physzool.66.4.30163803 ◽

1993 ◽

Vol 66 (4) ◽

pp. 455-473 ◽

Cited By ~ 71

Author(s):

In-Ho Choi ◽

Robert E. Ricklefs ◽

Russell E. Shea

Keyword(s):

Skeletal Muscle ◽

Enzyme Activities ◽

Muscle Growth ◽

Skeletal Muscle Growth ◽

Precocial Birds

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Anemic Hypoxemia Reduces Myoblast Proliferation and Muscle Growth in Late Gestation Fetal Sheep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00342.2020 ◽

2021 ◽

Author(s):

Paul J. Rozance ◽

Stephanie R Wesolowski ◽

Sonnet S. Jonker ◽

Laura D Brown

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Muscle Growth ◽

Late Gestation ◽

Whole Body ◽

Myoblast Differentiation ◽

Fetal Sheep ◽

Body Protein ◽

Skeletal Muscle Growth ◽

Myoblast Proliferation

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.

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