The effect of aspartate on the energy metabolism in the liver of weanling pigs challenged with lipopolysaccharide.

Autor: Kang, Ping, Liu, Yulan, Zhu, Huiling, Li, Shuang, Shi, Haifeng, Chen, Feng, Leng, Weibo, Pi, Dinan, Hou, Yongqing, Yi, Dan
Předmět:
Zdroj: European Journal of Nutrition; Jun2015, Vol. 54 Issue 4, p581-588, 8p
Abstrakt: Purpose: This study was conducted to investigate whether aspartate (Asp) could improve liver energy status in the lipopolysaccharide (LPS)-challenged pigs. Methods: Twenty-four weaned pigs were assigned to four treatments: (1) nonchallenged control (control diet and saline-treated); (2) LPS-challenged control (the same control diet and LPS-challenged); (3) LPS + 0.5 % Asp treatment (0.5 % Asp diet and LPS-challenged); and (4) LPS + 1.0 % Asp treatment (a 1.0 % Asp diet and LPS-challenged). On d 19, the pigs were injected intraperitoneally with Escherichia coli LPS at 100 μg/kg body weight, and the same volume of 0.9 % NaCl solution, respectively. All pigs were slaughtered at 24 h after LPS or saline injection, and the liver was collected for further analysis. Results: Dietary supplementation with Asp improved liver energy status evidenced by the increased ATP concentration and adenylate energy charges, and the decreased AMP concentration and AMP/ATP ratio ( p < 0.05). Asp supplementation increased the mRNA expression of key enzymes in hepatic glycolysis and tricarboxylic acid (TCA) cycle, including pyruvate kinase and citrate synthase ( p < 0.05), and had a tendency to increase hepatic pyruvate dehydrogenase and isocitrate dehydrogenase β mRNA expression ( p < 0.10). In addition, Asp increased the mRNA expressions of hepatic AMP-activated protein kinase (AMPK) α1, AMPKα2, silent information regulator (Sirt1), and proliferator-activated receptor-γ coactivator 1α (PGC1α) ( p < 0.05). Moreover, Asp increased AMPKα phosphorylation ( p < 0.05). Conclusions: These results indicated that dietary supplementation of Asp could improve energy status in LPS-injured liver, which might result from motivating the metabolism pathway of TCA cycle and glycolysis and stimulating the AMPK signaling pathway. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index