1. The experiment was conducted to investigate the effects of dietary sodium butyrate on the growth performance and immune response of broiler chickens. In experiment 1, 240 1-d-old chickens were allocated into 4 dietary groups (0, 0·25, 0·50 or 1·00 g sodium butyrate/kg) with 6 replicates each. In experiment 2, 120 1-d-old chickens were fed a control diet (without sodium butyrate) or 1·00 g sodium butyrate/kg diet. Half of the chickens fed on each diet were injected intra-peritoneally with 0·5 g/kg body weight of Escherichia coli lipopolysaccharide (LPS) at 16, 18 and 20 d of age. 2. There was no effect of dietary sodium butyrate on growth performance. On d 21, serum interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) were decreased in chickens given 1·00 g sodium butyrate/kg, serum superoxide dismutase (SOD) and catalase activities were significantly increased, and malondialdehyde (MDA) was decreased by dietary sodium butyrate at 0·50 or 1·00 g/kg. On d 42, serum IL-6 was markedly decreased by dietary sodium butyrate, while 1·00 g sodium butyrate/kg greatly reduced MDA and increased catalase. 3. LPS challenge significantly reduced the growth performance of chickens. Serum IL-1β, IL-6, TNF-α, corticosterone, alpha-1 acid glycoprotein (AGP) and prostaglandin E₂ (PGE₂) were increased in LPS-challenged chickens. Dietary sodium butyrate supplementation maintained the body weight gain and feed intake. Sodium butyrate supplementation inhibited the increase in IL-6 and AGP in serum at 16 d of age and TNF-α, corticosterone, AGP and PGE₂ at 20 d of age. Similar inhibitory effects of sodium butyrate in serum glucose and total protein concentrations were also found at 20 d of age. 4. The results indicated that dietary sodium butyrate supplementation can improve the growth performance in chickens under stress and that this may be used to moderate the immune response and reduce tissue damage.

Heat stress impairs growth performance and alters body protein and amino acid metabolism. This study was investigated to explore how body protein and amino acid metabolism changed under heat stress (HS) and the stress adaptation mechanism. A total of 144 broilers (28 d old) were divided into 3 treatment groups for 1 wk: HS group (32°C), normal control group (22°C), and pair-feeding group (22°C). We found that HS elevated the feed-to-gain ratio, reduced the ADFI and ADG, decreased breast muscle mass and plasma levels of several amino acids (glycine, lysine, threonine, and tyrosine), and increased serum glutamic oxaloacetic transaminase (GOT) activity and corticosterone (CORT) level and liver GOT and glutamic pyruvic transaminase activities. Heat stress elevated muscle atrophy F-box mRNA expression and reduced mRNA expression of the 70-kD ribosomal protein S6 kinase in the breast muscle of broilers. Broilers in the HS group exhibited striking increases of mRNA expressions of solute carrier family 1 member 1, family 3 member 1, family 7 member 1, and family 7 member-like in the liver and liver gluconeogenesis genes (PCKc, PCKm, PC, and FBP1) in comparison with the other 2 groups. In conclusion, HS increased the circulating CORT level and subsequently caused muscle protein breakdown to provide amino acid substrates to liver gluconeogenesis responsible for energy supply.

Chronic heat stress can enhance fat synthesis in broilers, and excessive triglyceride (TG) synthesized by the liver needs to be transported to extrah

Liver is a central metabolic organ, which is sensitive to heat stress. Liver damage affects animals' health and endangers the livestock and poultry industry. This study aimed to investigate the mechanism of chronic heat stress-induced liver damage in broiler chickens. Broilers were divided into 3 treatments: normal control group (NOR, 22°C), heat stress group (HS, 32°C) and pair-feeding group (PF, 22°C) for a 7-d and 14-d trial. The results showed that 7 d heat exposure caused microvesicular steatosis and reduced glutamine synthetase activity in broiler liver (P < 0.05). After 14 d of heat exposure, heat stress caused vacuolar degeneration and apoptosis in the liver; elevated liver relative weight and liver glutaminase activity as well as plasma ammonia level (P < 0.05). Additionally, heat stress enhanced GRP78 protein expression and the mRNA expressions of endoplasmic reticulum (ER) stress responses genes and apoptosis-related genes in broiler liver after 14 d of heat exposure (P < 0.05). In conclusion, chronic heat stress triggered ER stress-induced apoptosis and caused liver damage, which may compromise ammonia detoxification in broiler liver.