We investigated the molecular mechanisms by which chronic heat stress impairs the breast-meat quality of broilers. Broilers were assigned to three groups: the normal control (NC) group, heat-stress (HS) group, and pair-fed (PF) group. After 7 days of heat exposure (32 °C), the high temperature had caused oxidative stress; elevated the activity of citrate synthase (CS), the mRNA expression of M-CPT1, and the phosphorylation level of AMPKα; and reduced the mRNA expression of avUCP. After 14 days of heat exposure, the heat stress had increased the lightness and drip loss and decreased the pH and shear force of the breast meat. Additionally, the heat exposure had increased the mRNA expressions of FAS, ACC, and PDK4; the content of lipids; and the activities of lactic dehydrogenase and pyruvate kinase, and it had decreased the mRNA expression of M-CPT1 and the activity of CS. In conclusion, chronic heat stress impairs meat quality by causing mitochondria to malfunction and affecting energy-substance aerobic metabolism, resulting in increased glycolysis and intramuscular fat deposition.
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.
Heat stress markedly impairs the growth performance of broilers, such as the reduction of breast muscle mass and yield. The aim of this study was to examine the molecular mechanism of depressed muscle mass and yield caused by heat stress. A total of 144 (28-day-old) male broilers were allocated randomly into 3 treatment groups: (1) the normal control group (environment temperature was 22°C), (2) the heat stress group (environment temperature was 32°C), (3) the pair-fed group (environment temperature was 22°C and pair-fed to heat stress group). The experiment lasted for 14 d (from the age of 28 to 42 d). After 14 d of heat exposure, heat stress decreased (P < 0.05) broiler average daily gain, breast muscle mass, and muscle yield, and increased (P < 0.05) feed to gain ratio. After 14 d of heat exposure, heat stress increased (P < 0.05) the activities of aspartate aminotransferase and the concentrations of uric acid and most amino acids in serum, and reduced (P < 0.05) the concentration of insulin like growth factor 1 (IGF-1) in serum. Additionally, heat stress decreased (P < 0.05) the mRNA expressions of IGF-1, IGF-1 receptor, insulin receptor substrate 1, mammalian target of rapamycin (mTOR), the 70 kD ribosomal protein S6 kinase, myogenic differentiation, myogenin, solute carrier family 38 member 2, solute carrier family 7 member 5, and solute carrier family 3 member 2 of the breast muscle. In conclusion, chronic heat stress resulted in lower breast muscle mass and yield, and decreased muscle protein synthesis and amino acid transportation by downregulating IGFs-mTOR signal pathway. These findings have important practical significance in discovering effective means to alleviate muscle loss caused by chronic heat stress.
To investigate the effects of heat stress on broiler metabolism, we assigned 144 broilers to normal control (NC), heat stress (HS) or pair-fed (PF) groups and then monitored the effects using growth performance, carcass characteristics, biochemical assays and GC-MS-based metabolomics. The up-regulation of cloacal temperature confirmed that our experiment was successful in inducing chronic heat stress. The average daily gain and average daily feed intake of the HS group were significantly lower than those of the NC group, by 28·76 and 18·42 %, respectively (P1 and P<0·05). The greater feed:gain ratio of the HS group was significantly positively correlated with the leg, abdominal fat, subcutaneous fat and intramuscular fat proportions and levels of some free amino acids (proline, l-cysteine, methionine and threonine) but was negatively correlated with breast proportion and levels of some NEFA (stearic acid, arachidonic acid, palmitic acid and oleic acid). These findings indicated that the heat-stressed broilers were in negative energy balance and unable to effectively mobilise fat, thereby resulting in protein decomposition, which subsequently affected growth performance and carcass characteristics.
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