Thirty‐two 15‐day old broiler chicks (Chunky strain ROSS 308) were randomly divided into four treatments in a 2 × 2 factorial design. The main factors were diet (basal diet or basal diet supplemented with 0.15% astaxanthin‐rich dried cell powder (Panaferd‐P [astaxanthin 30 ppm]) and ambient temperature (thermo‐neutral [25 ± 1°C] or high [35 ± 1°C for 6 hr]). Dietary supplementation with Panaferd‐P did not affect growth performance, though high ambient temperature decreased feed intake and the weight of breast tender muscle, liver, and heart. High ambient temperature also decreased redness in both breast and leg muscles of chickens, while Panaferd‐P increased redness and yellowness of breast and leg muscles of chickens. Panaferd‐P increased Paracoccus carotinifaciens‐derived pigments (i.e., adonixanthin, astaxanthin, adonirubin, and cantaxanthin) as well as corn‐derived pigments such as zeaxanthin and lutein in breast and leg muscles. High ambient temperature increased the malondialdehyde (MDA) concentration in breast muscle, while Panaferd‐P decreased the MDA concentration in breast muscle under both temperature conditions. Our results suggest that dietary supplementation with Panaferd‐P increases muscle carotenoid content, the redness and yellowness of meat and decreases the muscle MDA concentration in broiler chickens kept under thermo‐neutral or high ambient temperature conditions.

The aim of this study was to evaluate the effects of high ambient temperature (HT) and orotic acid supplementation on the plasma and muscle metabolomic profiles in broiler chickens. Thirty-two 14-day-old broiler chickens were divided into four treatment groups that were fed diets with or without 0.7% orotic acid under thermoneutral (25 ± 1 °C) or cyclic HT (35 ± 1 °C for 8 h/day) conditions for 2 weeks. The chickens exposed to HT had higher plasma malondialdehyde concentrations, suggesting an increase in lipid peroxidation, which is alleviated by orotic acid supplementation. The HT environment also affected the serine, glutamine, and tyrosine plasma concentrations, while orotic acid supplementation affected the aspartic acid, glutamic acid, and tyrosine plasma concentrations. Untargeted gas chromatography–triple quadrupole mass spectrometry (GC-MS/MS)-based metabolomics analysis identified that the HT affected the plasma levels of metabolites involved in purine metabolism, ammonia recycling, pyrimidine metabolism, homocysteine degradation, glutamate metabolism, urea cycle, β-alanine metabolism, glycine and serine metabolism, and aspartate metabolism, while orotic acid supplementation affected metabolites involved in pyrimidine metabolism, β-alanine metabolism, the malate–aspartate shuttle, and aspartate metabolism. Our results suggest that cyclic HT affects various metabolic processes in broiler chickens, and that orotic acid supplementation ameliorates HT-induced increases in lipid peroxidation.

To investigate the intracellular signaling mechanisms by which clenbuterol reduces muscle protein degradation, we examined the phosphorylation level and intracellular localization of FOXO1 in the sartorius muscle of neonatal chicks. One-day-old chicks were given a single intraperitoneal injection of clenbuterol (0.1 mg/kg body weight). Three hours after injection, AKT protein was phosphorylated in the sartorius muscle by clenbuterol injection. Coincidentally, clenbuterol increased cytosolic level of phosphorylated FOXO1 protein, while it decreased nuclear level of FOXO1 protein in the sartorius muscle. Furthermore, clenbuterol decreased the expression of mRNAs for muscle-specific ubiquitin ligases (atrogin-1/MAFbx and MuRF1) in the sartorius muscle accompanied by decreased plasma 3-methylhistidine concentration, an index of muscle protein degradation, at 3 h after injection. These results suggested that, in the sartorius muscle of the chicks, clenbuterol changed the intracellular localization of phosphorylated FOXO1, and consequently decreased protein degradation via suppressing the expression of genes encoding muscle-specific ubiquitin ligases.