scholarly journals Mitochondrial phosphoenolpyruvate carboxykinase (PEPCK-M) and serine biosynthetic pathway genes are co-ordinately increased during anabolic agent-induced skeletal muscle growth

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
D. M. Brown ◽  
H. Williams ◽  
K. J. P. Ryan ◽  
T. L. Wilson ◽  
Z. C. T. R. Daniel ◽  
...  
2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 287-288
Author(s):  
Laura A Smith ◽  
Nikole E Ineck ◽  
Brynne A Udy ◽  
Chris L Erickson ◽  
Kara J Thornton

Abstract Androgens, such as testosterone, increase growth of skeletal muscle, although the exact mechanism through which these molecules function to increase growth of skeletal muscle remains unknown. Recent research indicates that one of the mechanisms through which androgens improve skeletal muscle growth is by modulation of the polyamine biosynthetic pathway. Polyamines are naturally occurring amino acid derivatives that are found in many whole foods and are potent stimulators of cell proliferation. However, the effect that polyamines have on growth of skeletal muscle has not been well characterized. The objective of this study was to investigate the effect that trenbolone acetate (a testosterone analog, TBA), polyamines (putrescine, spermine, and spermidine), and polyamine precursors (methionine and ornithine) have on proliferation of Sol8 and C2C12 murine myoblasts. Cultures were treated with 1% fetal bovine serum and 10 nM TBA, 10 mM methionine, 8 mM ornithine, 3 mM putrescine, 1.5 mM spermidine, or 0.1 mM spermine and proliferation rates were compared to a control (1% fetal bovine serum). Sol8 cells that were treated with 10 nM TBA, 10 mM methionine, 8 mM ornithine, 3 mM putrescine, 1.5 mM spermidine, or 0.1 mM spermine had increased (P < 0.05) proliferation rates compared to the control. C2C12 cells that were treated with 10 nM TBA or 10 mM methionine had increased (P < 0.05) proliferation rates compared to the control. This research demonstrates that TBA, some polyamines, and some polyamine precursors increase proliferation of myoblasts and thus, are capable of enhancing the rate of skeletal muscle growth. However, further research is needed to understand the relationship between androgens and the polyamine biosynthetic pathway relative to skeletal muscle growth.


2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 234-234
Author(s):  
Laura A Smith ◽  
Nikole E Ineck ◽  
Brynne A Udy ◽  
Chris L Erickson

Abstract Androgens, such as testosterone, increase growth of skeletal muscle, although the exact mechanism through which these molecules function to increase growth of skeletal muscle remains unknown. Recent research indicates that one of the mechanisms through which androgens improve skeletal muscle growth is by modulation of the polyamine biosynthetic pathway. Polyamines are naturally occurring amino acid derivatives that are found in many whole foods and are potent stimulators of cell proliferation in several different cell types. However, the effect that polyamines have on growth of skeletal muscle has not been well characterized. The objective of this study was to investigate the effect that trenbolone acetate (a testosterone analog, TBA), polyamines (putrescine, spermine, and spermidine), and polyamine precursors (methionine and ornithine) have on proliferation of Sol8 and C2C12 murine myoblasts. Cultures were treated with 1% fetal bovine serum and 10 nM TBA, 10 mM methionine, 8 mM ornithine, 3 mM putrescine, 1.5 mM spermidine, or 0.5 mM spermine and proliferation rates were compared to a control (1% fetal bovine serum). Sol8 cells that were treated with 10 nM TBA and 10 mM methionine had increased (P < 0.001) proliferation rates compared to the control. C2C12 cells that were treated with 10 nM TBA, 8 mM ornithine, or 1.5 mM spermidine had increased (P < 0.001) proliferation rates compared to the control. This research demonstrates that TBA, some polyamines, and some polyamine precursors increase proliferation of myoblasts and thus, are capable of enhancing the rate of skeletal muscle growth. However, further research is needed to understand the relationship between androgens and the polyamine biosynthetic pathway relative to skeletal muscle growth.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 334-334
Author(s):  
Zhi-wen Song ◽  
Cheng-long Jin ◽  
Mao Ye ◽  
Chun-qi Gao ◽  
Hui-chao Yan ◽  
...  

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.


Author(s):  
Paul J. Rozance ◽  
Stephanie R Wesolowski ◽  
Sonnet S. Jonker ◽  
Laura D Brown

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.


2017 ◽  
Vol 293 (1) ◽  
pp. 69-80 ◽  
Author(s):  
Zhenhui Li ◽  
Bahareldin Ali Abdalla ◽  
Ming Zheng ◽  
Xiaomei He ◽  
Bolin Cai ◽  
...  

Development ◽  
2018 ◽  
Vol 145 (20) ◽  
pp. dev167197 ◽  
Author(s):  
John F. Bachman ◽  
Alanna Klose ◽  
Wenxuan Liu ◽  
Nicole D. Paris ◽  
Roméo S. Blanc ◽  
...  

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