تأثیر تنش گرمایی ملایم و مزمن بر عملکرد، خصوصیات لاشه، فراسنجه‌های خونی، کیفیت گوشت و بیان ژن‌های اسیدچرب سنتاز و لیپوپروتئین لیپازدر جوجه‌های گوشتی

Introduction: Heat stress as one of the most challenging environmental stresses can growth performance. Broilers are sensitive to heat stress due to the lack of sweat glands. The temperature range for most poultry species is between 16 and 26 degrees Celsius. Heat stress reduces welfare, growth performance, high mortality and large economic losses changes in carcass composition, lipid profile and lipolytic capacity are high under heat stress conditions because heat stress causes significant increases in catabolic and stress hormones (epinephrine, cortisol, and glucagon). Jestrbesk et al. (2017) reported that heat stress increases the activity of fatty acid synthetase (which converts malonyl-CoA to acyl-ACP and acyl-ACP to myristat or palmitate), acetyl cocarboxylase (which it converts acetyl-CoA to malonyl-CoA) and acyl-coasynthetase (which converts myristate to myristate-CoA and palmitate to palmitate-CoA). Liver and adipose tissue are rich in fatty acid synthase, but more than 90% of fatty acid is synthesized in the liver of broiler chickens, and adipose tissue is only responsible for storage (Ijiri et al. 2016). Heat stress, through the increase of lipoprotein lipase in adipose tissue of animals, increases the capacity to harvest and store intestinal and liver-derived triglyceride in adipose tissue (Lu et al. 2007).
Material and Methods: The present study was performed to investigate the effect of mild and chronic heat stress on growth performance, carcass traits, blood parameters, meat quality and relative expression of broiler fatty acid synthase and lipoprotein lipase genes. For this purpose, 150 one-day-old male broilers of Ross 308 strain in a completely randomized design with 3 treatments (normal temperature (according to the recommendation of Ross 308 strain), mild stress (27 °C) and chronic stress (32 °C), 5 replicates and 10 birds were kept in each replication from 1 to 42 days. The diet was based on corn and soybean meal and formulated according Ross (308) requirements for three period of starter (1-10 d), growth (11-24 d) and finisher (25-42 d) days. Body weight gain and feed intake was measured periodically and calculated during the whole experiment on a pen basis, and the feed conversion ratio was calculated subsequently. At day 42 of age, two birds per pen were randomly selected, weighed, and slaughtered. After slaughter, percentage of carcass, breast, thigh, abdominal fat, pancreas, liver, heart, bursa of fabricius and spleen were calculated as a ratio of the live weight. To determine the meat quality, 50g of left breast muscle was collected in plastic bags and stored at a negative temperature of 20°C. Meat quality parameters including water holding capacity, moisture, ash, pH, fat, protein, malondialdehyde and total antioxidant activity were measured. Data were analyzed using the general Linear Model procedures of SAS 9.1. When the analysis of variance was significant, Duncan's multiple-range test was used to separate the means. Statements of statistical significance were based on P<0.05.
Results and Discussion: The results showed that the weight gain of chicks under chronic heat stress in the final period (25 to 42 days) and the whole period (1 to 42 days) was lower than chickens under normal temperature (P <0.05). Exposure to chronic heat stress significantly increased the relative weight of abdominal fat, plasma glucose and triglycerides, and malondialdehyde of broiler breast meat (P <0.05).In agreement with the present result, El-Husseiny and Krieger (1980) also reported that the abdominal fat of broiler chickens under 32 degrees Celsius temperature was more than that of chickens raised at 22 degrees Celsius. Mujahid et al. (2007) stated that heat stress increases plasma levels of fatty acids, triglycerides and cholesterol. The increase of these parameters is probably due to the release of glucocorticoids and the movement of fats, especially triglycerides from the tissues. In agreement with the present result, Lu et al. (2017) reported an increase in the level of malondialdehyde in the breast meat of broilers exposed to chronic heat stress. Heat stress leads to the creation of oxidative stress by increasing the production of free radicals, and the oxidative stress created during heat stress causes an increase in the level of malondialdehyde in skeletal muscles (Vosough-Ghanbari et al. 2010).Chronic heat stress also increased the relative expression of broiler lipoprotein lipase gene in broiler chickens (P <0.05). The relative expression of fatty acid synthase gene also increased significantly in the liver of birds exposed to mild and chronic heat stress (P <0.05). Fatty acid synthase is the limiting enzyme in last step of the synthesis of long-chain fatty acids in animals and the catalysis of acetyl-CoA and malonyll-CoA to fatty acids (Smith 2003). Fatty acid synthesized by liver are incorporated into triacyllglycerols and transported as very low- density lipoproteins (VLDL), which provide this key energy source for other tissues for immediate use or provides storage (Flees et al. 2017).Studies suggest that under stress conditions, high levels of corticosterone and plasma insulin can increase the expression level of LXRa mRNA, which in turn activates the expression of liver SREBp-LC mRNA (Janowski et al. 1999). Therefore, LXRa and SREBp-LC can activate the transfer of key genes required for fat synthesis, such as fatty acid synthase and acetyl cocarboxylase (Demeure et al. 2009). Lu et al. (2007) stated that chronic heat stress negatively affects fat storage and meat quality in broiler chickens, and through the increase of lipoprotein lipase in the adipose tissue of animals, it increases the capacity of harvesting and storing intestinal and liver-derived triglycerides in fat tissue.
Conclusion: In general, exposure to chronic heat stress further decreased yield and increased carcass fat and increased the relative expression of fatty acid synthase genes in the liver and lipoprotein lipase in the breast.