Lysine inhibits apoptosis in satellite cells to govern skeletal muscle growth via the JAK2-STAT3 pathway.

Apoptosis is programmed cell death that can be stimulated by external stress or nutrition restrictions. However, the precise mechanism of apoptosis in skeletal muscle remains unknown. The objective of this study was to investigate whether apoptosis could be regulated by lysine (Lys) supplementation and the potential mechanism. In this study, an isobaric tag for relative and absolute quantification (iTRAQ) proteomics analysis of the longissimus dorsi muscle from piglets showed that the 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 demonstrated that Lys deficiency led to apoptosis in the longissimus dorsi muscle with the JAK2-STAT3 pathway inhibition. Interestingly, apoptosis was suppressed, and the JAK2-STAT3 pathway was reactivated after Lys re-supplementation. In addition, the results showed that Lys deficiency-induced apoptosis in satellite cells (SCs) was mediated by the JAK2-STAT3 pathway inhibition. Moreover, the JAK2-STAT3 pathway was reactivated by Lys re-supplementation and suppressed cell apoptosis, and this effect was inhibited after treatment with Tyrphostin B42 (AG 490). In conclusion, we found that Lys inhibits apoptosis in SCs to govern skeletal muscle growth via the JAK2-STAT3 pathway.

mTORC1-Mediated Satellite Cell Differentiation Is Required for Lysine-Induced Skeletal Muscle Growth.

Skeletal muscle is the primary source of protein for humans. However, the mechanisms of skeletal muscle growth, such as nutrition control, remain unknown. Moreover, the function of lysine (Lys) in controling skeletal muscle growth has gradually demonstrated that Lys is not only substantial for protein synthesis but also a signaling molecule for satellite cell (SC) activation. In the current work, the number of differentiated SCs in the longissimus thoracis muscle and the fusion index of SCs were both governed by Lys supplementation. Meanwhile, the myogenic regulatory factors and the mammalian target of rapamycin complex 1 (mTORC1) pathway showed the same tendencies of changes as the differentiation of SCs. After Lys was resupplemented with rapamycin, the mTORC1 pathway was inhibited and the differentiation ability of SCs was suppressed. Collectively, the results showed that the mTORC1-pathway-mediated SC differentiation was required for Lys-promoted skeletal muscle growth.

Effects of nitrate concentration in interstitial water on the bioremediation of simulated oil-polluted shorelines.

Nutrient addition has been proved to be an effective strategy to enhance oil biodegradation in marine shorelines. To determine the optimal range of nutrient concentrations in the bioremediation of oil-polluted beaches, nitrate was added to the simulated shoreline models in the initial concentration of 1, 5 and 10 mg/L. Whenever the NO3-N concentration declined to 70% of its original value, additional nutrients were supplemented to maintain a certain range. Results showed adding nutrients increased the oil biodegradation level, the counts of petroleum degrading bacteria (PDB) and heterotrophic bacteria (HB), and the promoted efficiency varied depending on the concentration of nitrate. Oil degradation level in 5 mg/L (NO3-N) group reached as much as 84.3% accompanied with the consistently highest counts of PDB; while in 1 mg/L group oil removal efficiency was only 35.2%, and the numbers of PDB and HB were relatively low compared to the other groups supplemented with nutrients. Although counts of HB in the 10 mg/L group were remarkable, lower counts of PDB resulted in poorer oil removal efficiency (70.5%) compared to 5 mg/L group. Furthermore, it would need more NO3-N (0.371 mg) to degrade 1 mg diesel oil in the 10 mg/L group than in the 5 mg/L group (0.197 mg). In conclusion, Nitrate concentration in 5 mg/L is superior to 1 and 10 mg/L in the enhancement of diesel oil biodegradation in simulated shorelines.

Degradation of crude oil by indigenous microorganisms supplemented with nutrients.

Different kinds of mineral nutrients(NO3-N, NH4-N and PO4-P) were applied in the simulated oil-polluted seawater for enhancing oil biodegradation in the N/P ratio 10:1 and 20:1. Although indigenous microorganisms have the ability to degrade oil, adding nutrients accelerated biodegradation rates significantly. For the group amended with NO3-N and PO4-P in the ratio 10:1, the reaction rate coefficient was 4 times higher than the natural biodegradation. Chemical and microbiological analysis showed that the optimal N/P ratio in the system is 10:1, and microorganisms tend to utilize nitrate rather than ammonium as N source.