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Asparagine reduces the mRNA expression of muscle atrophy markers via regulating protein kinase B (Akt), AMP-activated protein kinase α, toll-like receptor 4 and nucleotide-binding oligomerisation domain protein signalling in weaning piglets after lipopolysaccharide challenge.
Br J Nutr. 2016 Oct; 116(7):1188-1198.BJ

Abstract

Pro-inflammatory cytokines are critical in mechanisms of muscle atrophy. In addition, asparagine (Asn) is necessary for protein synthesis in mammalian cells. We hypothesised that Asn could attenuate lipopolysaccharide (LPS)-induced muscle atrophy in a piglet model. Piglets were allotted to four treatments (non-challenged control, LPS-challenged control, LPS+0·5 % Asn and LPS+1·0 % Asn). On day 21, the piglets were injected with LPS or saline. At 4 h post injection, piglet blood and muscle samples were collected. Asn increased protein and RNA content in muscles, and decreased mRNA expression of muscle atrophy F-box (MAFbx) and muscle RING finger 1 (MuRF1). However, Asn had no effect on the protein abundance of MAFbx and MuRF1. In addition, Asn decreased muscle AMP-activated protein kinase (AMPK) α phosphorylation, but increased muscle protein kinase B (Akt) and Forkhead Box O (FOXO) 1 phosphorylation. Moreover, Asn decreased the concentrations of TNF-α, cortisol and glucagon in plasma, and TNF-α mRNA expression in muscles. Finally, Asn decreased mRNA abundance of muscle toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) signalling-related genes, and regulated their negative regulators. The beneficial effects of Asn on muscle atrophy may be associated with the following: (1) inhibiting muscle protein degradation via activating Akt and inactivating AMPKα and FOXO1; and (2) decreasing the expression of muscle pro-inflammatory cytokines via inhibiting TLR4 and NOD signalling pathways by modulation of their negative regulators.

Authors+Show Affiliations

1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.2Laboratory of Developmental Nutrition,Department of Animal Science,North Carolina State University,Raleigh,NC 27695,USA.2Laboratory of Developmental Nutrition,Department of Animal Science,North Carolina State University,Raleigh,NC 27695,USA.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27572423

Citation

Wang, Xiuying, et al. "Asparagine Reduces the mRNA Expression of Muscle Atrophy Markers Via Regulating Protein Kinase B (Akt), AMP-activated Protein Kinase Α, Toll-like Receptor 4 and Nucleotide-binding Oligomerisation Domain Protein Signalling in Weaning Piglets After Lipopolysaccharide Challenge." The British Journal of Nutrition, vol. 116, no. 7, 2016, pp. 1188-1198.
Wang X, Liu Y, Wang S, et al. Asparagine reduces the mRNA expression of muscle atrophy markers via regulating protein kinase B (Akt), AMP-activated protein kinase α, toll-like receptor 4 and nucleotide-binding oligomerisation domain protein signalling in weaning piglets after lipopolysaccharide challenge. Br J Nutr. 2016;116(7):1188-1198.
Wang, X., Liu, Y., Wang, S., Pi, D., Leng, W., Zhu, H., Zhang, J., Shi, H., Li, S., Lin, X., & Odle, J. (2016). Asparagine reduces the mRNA expression of muscle atrophy markers via regulating protein kinase B (Akt), AMP-activated protein kinase α, toll-like receptor 4 and nucleotide-binding oligomerisation domain protein signalling in weaning piglets after lipopolysaccharide challenge. The British Journal of Nutrition, 116(7), 1188-1198.
Wang X, et al. Asparagine Reduces the mRNA Expression of Muscle Atrophy Markers Via Regulating Protein Kinase B (Akt), AMP-activated Protein Kinase Α, Toll-like Receptor 4 and Nucleotide-binding Oligomerisation Domain Protein Signalling in Weaning Piglets After Lipopolysaccharide Challenge. Br J Nutr. 2016;116(7):1188-1198. PubMed PMID: 27572423.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Asparagine reduces the mRNA expression of muscle atrophy markers via regulating protein kinase B (Akt), AMP-activated protein kinase α, toll-like receptor 4 and nucleotide-binding oligomerisation domain protein signalling in weaning piglets after lipopolysaccharide challenge. AU - Wang,Xiuying, AU - Liu,Yulan, AU - Wang,Shuhui, AU - Pi,Dingan, AU - Leng,Weibo, AU - Zhu,Huiling, AU - Zhang,Jing, AU - Shi,Haifeng, AU - Li,Shuang, AU - Lin,Xi, AU - Odle,Jack, Y1 - 2016/08/30/ PY - 2016/8/31/pubmed PY - 2017/5/26/medline PY - 2016/8/31/entrez KW - AMPK AMP-activated protein kinase KW - Akt protein kinase B KW - Asn asparagine KW - CENTB1 centaurin β1 KW - CONTR non-challenged control KW - FOXO Forkhead Box O KW - GAPDH glyceraldehyde 3-phosphate dehydrogenase KW - LD longissimus dorsi KW - LPS lipopolysaccharide KW - MAFbx muscle atrophy F-box KW - MuRF1 muscle RING finger 1 KW - MyD88 myeloid differentiation factor 88 KW - NOD nucleotide-binding oligomerisation domain protein KW - RP105 radioprotective 105 KW - SOCS1 suppressor of cytokine signalling 1 KW - TLR toll-like receptor KW - Tollip toll-interacting protein KW - pAMPKα phosphorylated AMPKα KW - pAkt phosphorylated Akt KW - tAMPKα total AMPKα KW - tAkt total Akt KW - tFOXO1 total FOXO 1 KW - Asparagine KW - Lipopolysaccharides KW - Muscle atrophy KW - Pro-inflammatory cytokines SP - 1188 EP - 1198 JF - The British journal of nutrition JO - Br. J. Nutr. VL - 116 IS - 7 N2 - Pro-inflammatory cytokines are critical in mechanisms of muscle atrophy. In addition, asparagine (Asn) is necessary for protein synthesis in mammalian cells. We hypothesised that Asn could attenuate lipopolysaccharide (LPS)-induced muscle atrophy in a piglet model. Piglets were allotted to four treatments (non-challenged control, LPS-challenged control, LPS+0·5 % Asn and LPS+1·0 % Asn). On day 21, the piglets were injected with LPS or saline. At 4 h post injection, piglet blood and muscle samples were collected. Asn increased protein and RNA content in muscles, and decreased mRNA expression of muscle atrophy F-box (MAFbx) and muscle RING finger 1 (MuRF1). However, Asn had no effect on the protein abundance of MAFbx and MuRF1. In addition, Asn decreased muscle AMP-activated protein kinase (AMPK) α phosphorylation, but increased muscle protein kinase B (Akt) and Forkhead Box O (FOXO) 1 phosphorylation. Moreover, Asn decreased the concentrations of TNF-α, cortisol and glucagon in plasma, and TNF-α mRNA expression in muscles. Finally, Asn decreased mRNA abundance of muscle toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) signalling-related genes, and regulated their negative regulators. The beneficial effects of Asn on muscle atrophy may be associated with the following: (1) inhibiting muscle protein degradation via activating Akt and inactivating AMPKα and FOXO1; and (2) decreasing the expression of muscle pro-inflammatory cytokines via inhibiting TLR4 and NOD signalling pathways by modulation of their negative regulators. SN - 1475-2662 UR - https://www.unboundmedicine.com/medline/citation/27572423/Asparagine_reduces_the_mRNA_expression_of_muscle_atrophy_markers_via_regulating_protein_kinase_B__Akt__AMP_activated_protein_kinase_α_toll_like_receptor_4_and_nucleotide_binding_oligomerisation_domain_protein_signalling_in_weaning_piglets_after_lipopolysaccharide_challenge_ L2 - https://www.cambridge.org/core/product/identifier/S000711451600297X/type/journal_article DB - PRIME DP - Unbound Medicine ER -