Hepatic Injury Induced by Dietary Energy Level via Lipid Accumulation and Changed Metabolites in Growing Semi-Fine Wool Sheep

• Main Authors: Benchu Xue, Qionghua Hong, Xiang Li, Mingli Lu, Jia Zhou, Shuangming Yue, Zhisheng Wang, Lizhi Wang, Quanhui Peng, Bai Xue
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2021-09-01
• Series: Frontiers in Veterinary Science
• Subjects: liver; injury; metabonomics; energy level; oxidative stress
• Online Access: https://www.frontiersin.org/articles/10.3389/fvets.2021.745078/full

Liver injury threatens the overall health of an organism, as it is the core organ of the animal body. Liver metabolism is affected by numerous factors, with dietary energy level being a crucial one. Therefore, the present study aimed to evaluate hepatic injury and to describe its metabolic mechanism in ruminants fed diets with different dietary energy levels. A total of 25 Yunnan semi-fine wool sheep were fed diets with five dietary metabolic energy levels and were randomly assigned to five groups as follows: low energy (LE), medium–low energy (MLE), medium energy (ME), medium–high energy (MHE), and high energy (HE). The results revealed that the average optical density (AOD) of lipid droplets in the LE, MLE, and HE groups was higher than that in the ME and MHE groups. The enzyme activity of alanine aminotransferase (ALT) was the lowest in the ME group. An increase in dietary energy level promoted the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and altered the malondialdehyde (MDA) and protein carbonyl (PCO) concentration quadratically. In addition, both high and low dietary energy levels upregulated the mRNA abundance of proinflammatory cytokine interleukin (IL)-1β, nuclear factor-kappa B (NF-κB), and tumor necrosis factor (TNF)-α. Metabonomic analysis revealed that 142, 77, 65, and 108 differential metabolites were detected in the LE, MLE, MHE, and HE groups, compared with ME group respectively. These metabolites were involved in various biochemical pathways, such as glycolipid, bile acid, and lipid metabolism. In conclusion, both high and low dietary energy levels caused hepatic injury. Section staining and metabonomic results revealed that hepatic injury might be caused by altered metabolism and lipid accumulation induced by lipid mobilization.