Betaine Alleviates Heat Stress-Induced Hepatic and Mitochondrial Oxidative Damage in Broilers

The aim of this study was to evaluate the effects of dietary betaine (BET) on growth performance, redox state, and related gene expression in broilers under heat stress (HS). A total of 144 21-day-old male broiler chickens with similar body weights were assigned randomly to three treatments with six replicates (eight chickens per replicate cage). Broilers in the control (CON) group were kept at thermoneutral (TN, 22±1°C) conditions and fed a basal diet until they were 42 days of age. Broilers in the other two groups (defined as HS and HS + BET) were exposed to HS (34±1°C, 8 h/day) and fed the basal diet without or with 1000 mg/kg BET, respectively. Rectal and cockscomb temperature of broilers was increased (P<0.05) in HS and HS + BET groups compared with the CON group, whereas there was no difference between HS and HS + BET groups. Dietary BET supplementation restored (P<0.05) average daily gain (ADG) and average daily feed intake (ADFI) of broilers and reversed (P<0.05) the increase in serum alanine transaminase (ALT) activity and malondialdehyde (MDA) content in the liver tissue of broilers under HS. The HS + BET group had higher (P<0.05) activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the liver tissue and mitochondria than the HS group, and the same pattern was observed for glutathione (GSH) and GSH/glutathione disulphide (GSSG) in the liver tissue. The decreased mRNA levels of GPX1 and uncoupling protein (UCP) in the liver induced by HS were restored by BET supplementation. In conclusion, dietary BET supplementation can alleviate HS-induced hepatic and mitochondrial oxidative damage of broilers by regulating mRNA expressions of GPX1 and UCP.