Dietary Beta-Hydroxy Beta-Methyl Butyrate Supplementation Alleviates Liver Injury in Lipopolysaccharide-Challenged Piglets. (2nd April 2021)

• Record Type: Journal Article
• Authors: Duan, Yehui; Song, Bo; Zheng, Changbing; Zhong, Yinzhao; Guo, Qiuping; Zheng, Jie; Yin, Yulong; Li, Jianjun; Li, Fengna
• Other Names: Gebicki Janusz Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2021(2021)
• Publication Date: 2021-04-02
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2021/5546843
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : The current study was performed to investigate whether dietary β -hydroxy- β -methylbutyrate (HMB) could regulate liver injury in a lipopolysaccharide- (LPS-) challenged piglet model and to determine the mechanisms involved. Thirty piglets (21 ± 2 days old, 5.86 ± 0.18 kg body weight) were randomly divided into the control (a basal diet, saline injection), LPS (a basal diet), or LPS+HMB (a basal diet + 0.60% HMB-Ca) group. After 15 d of treatment with LPS and/or HMB, blood and liver samples were obtained. The results showed that in LPS-injected piglets, HMB supplementation ameliorated liver histomorphological abnormalities induced by LPS challenge. Compared to the control group, the activities of serum aspartate aminotransferase and alkaline phosphatase were increased in the LPS-injected piglets (P < 0.05 ). The LPS challenge also downregulated the mRNA expression of L-PFK, ACO, L-CPT-1, ICDH β, and AMPK α 1/2 and upregulated the mRNA expression of PCNA, caspase 3, TNF- α, TLR4, MyD88, NOD1, and NF- κ B p65 (P < 0.05 ). However, these adverse effects of the LPS challenge were reversed by HMB supplementation (P < 0.05 ). These results indicate that HMB may exert protective effects against LPS-induced liver injury, and the underlying mechanisms might involve the improvement of hepatic energy metabolism via regulating AMPK signaling pathway and the reduction of liver inflammation via modulating TLR4 and NOD signaling pathways.