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

卷:54

Kang, Ping ; Liu, Yulan ; Zhu, Huiling ; Li, Shuang ; Shi, Haifeng ; Chen, Feng ; Leng, Weibo ; Pi, Dinan ; Hou, Yongqing ; Yi, Dan

关键词: Aspartate;    Energy status;    Liver;    Piglets;    Lipopolysaccharide;   

DOI  :  10.1007/s00394-014-0739-3

学科分类：食品科学和技术

【 摘 要 】

This study was conducted to investigate whether aspartate (Asp) could improve liver energy status in the lipopolysaccharide (LPS)-challenged pigs. 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 mu g/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. 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 beta mRNA expression (p < 0.10). In addition, Asp increased the mRNA expressions of hepatic AMP-activated protein kinase (AMPK) alpha 1, AMPK alpha 2, silent information regulator (Sirt1), and proliferator-activated receptor-gamma coactivator 1 alpha (PGC1 alpha) (p < 0.05). Moreover, Asp increased AMPK alpha phosphorylation (p < 0.05). 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.