Selenogenome and AMPK signal insight into the protective effect of dietary selenium on chronic heat stress-induced hepatic metabolic disorder in growing pigs

Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein.

In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes that are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.

Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 °C) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 °C) with basal diet and supplied with 0.0, 0.2, 0.4, and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 d. The serum biochemical, hepatic metabolism related enzyme, protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR, ELISA and western blot.

CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, glycogen content, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA improved anti-oxidative capacity of liver. 0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight, glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver. Conclusions: In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes that are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.