|BECKFORD, RONIQUE - University Of Maryland|
|ELLESTAD, LAURA - University Of Maryland|
|FARLEY, LINDA - University Of Maryland|
|ANGEL, ROSALINA - University Of Maryland|
|LIU, HSAIO-CHING - North Carolina State University|
|PORTER, TOM - University Of Maryland|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/16/2020
Publication Date: 10/1/2020
Citation: Beckford, R., Ellestad, L.E., Proszkowiec-Wegla, M.K., Farley, L., Brady, K.M., Angel, R.C., Liu, H., Porter, T.E. 2020. Effects of heat stress on performance, blood chemistry and hypothalamic and pituitary mRNA expression in broiler chickens. Poultry Science. 99:6317–6325. https://doi.org/10.1016/j.psj.2020.09.052.
Interpretive Summary: As global temperatures continue to increase, poultry producers are challenged to find ways to alleviate the negative effects of heat stress on birds raised for meat and eggs. Heat stress in birds leads to decreased production in terms of egg produced or muscle growth, but can also lead to increased mortality. Despite the substantial impact of heat stress on poultry production, little is known about how birds respond to heat stress. The impact of heat stress on blood parameters, hormone levels, and gene expression of key responsive tissues was determined to characterize how this response is orchestrated at a physiological and molecular level. This study provides an overview of the avian response to heat stress, which can serve the poultry industry and future researchers as the baseline response to heat stress for potential heat stress mitigation projects.
Technical Abstract: This study was conducted to evaluate potential hormonal mechanisms associated with the stress response, thermoregulation, and metabolic changes of broiler chickens exposed to high environmental temperature. Nine hundred 1d old male broiler chicks (Ross 708) were placed in floor pens and raised to 24d. At 24d, chicks were randomly assigned to one of two treatments, heat stress (HS) or no heat stress (NHS), and allocated into battery cages in 4 batteries (10 birds/cage, 2 cages/treatment/battery). On d31, blood was collected prior to HS and analyzed using an iSTAT analyzer. Half of the batteries were then moved into two rooms with an elevated ambient temperature (35ºC) for 8h. Remaining batteries stayed in the thermoneutral rooms with an ambient temperature of 22ºC. Beginning 5h after the initiation of HS, blood was again collected and analyzed using an iSTAT analyzer, birds were euthanized, and hypothalamus and pituitary samples were collected (16 birds/treatment), flash frozen, and stored at -80o C until RNA extraction. Reverse transcription-quantitative PCR was used to compare mRNA levels of key corticotropic and thyrotrophic genes in the hypothalamus and pituitary. Levels of mRNA for each target gene were normalized to PGK1 (pituitary) and GAPDH (hypothalamus) mRNA. Differences were determined using mixed model ANOVA (SAS v9.4, Cary NC). Heat stress decreased (P < 0.05), feed intake, BW, bicarbonate, potassium, CO2, and triiodothyronine, while HS increased mortality, glucose, pH, plasma thyroxine, and corticosterone. Expression of pituitary corticotropin-releasing hormone receptor 1 was downregulated (P<0.001), while corticotropin-releasing hormone receptor 2 mRNA levels were higher (P=0.001) in HS birds. Heat stress increased expression of thyroid hormone receptor ß (P=0.01) (2.8-fold) and thyroid stimulating hormone ß (P=0.009) (1.4-fold). Heat stress did not affect levels of mRNA of genes evaluated in the hypothalamus. Results showed that HS significantly affected both the thyrotropic and corticotropic axes. Understanding the role and regulation of these pathways during HS will allow researchers to better evaluate management strategies to combat HS.