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 1-day-old male broiler chicks (Ross 708) were placed in floor pens and raised to 24 d. At 24 d, chicks were randomly assigned to 1 of 2 treatments, heat stress ( HS ) or no HS, and allocated into battery cages in 8 batteries (10 birds per cage, 2 cages per battery). On day 31, blood was collected prior to HS and analyzed using an iSTAT analyzer. Half of the batteries were then moved into 2 rooms with an elevated ambient temperature (35°C) for 8 h. The remaining batteries stayed in the thermoneutral rooms with an ambient temperature of 22°C. Beginning at 5 h after the initiation of HS, blood was collected and analyzed using an iSTAT analyzer, birds were euthanized, and hypothalamus and pituitary samples were collected (16 birds per treatment), flash frozen, and stored at −80°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. HS decreased ( P < 0.05) feed intake, BW, bicarbonate, potassium, CO 2 , and triiodothyronine, while it 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. HS increased expression of thyroid hormone receptor β ( P = 0.01) (2.8-fold) and thyroid stimulating hormone β ( P = 0.009) (1.4-fold). HS 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.

No abstract

The amount of corn available for animal and poultry feed has been unpredictable in recent years due to the increased use of corn for ethanol production. As a consequence, there has been an increase in the price of feed, chicken, and chicken products. Researchers are exploring alternative feed sources to substitute for corn in poultry ration. This study evaluated the performance and carcass quality of broilers fed diets containing sweet potato root meal (SPRM). After a complete nutrient analysis of the SPRM, diets were formulated where 0, 10, 20, and 30% of corn was substituted with SPRM. The study utilized 360 1-d-old Cornish X Rock male broiler chickens randomly assigned to one of 4 treatments; 0%, 10%, 20%, and 30% SPRM. Body weights and feed intake (FI) were monitored weekly for 7 wk. Birds were slaughtered on d 50 and FI, BW gain, ADG, ADFI, abdominal fat, dressing percentage, and organ weights measured. White (breast) and dark (leg and thigh) meat were evaluated for nutrient content (protein, moisture, fat, and ash). Results showed birds fed 20% SPRM had lower (P < 0.03) final BW, BW gain and ADG than those fed the 30% SPRM diet. There were no differences in FI and ADFI among treatments. Feed conversion ratio was lowest (P < 0.02) in birds fed 10, 20, and 30% SPRM than the control. There were no differences in dressing percentage among treatments. Abdominal fat was highest (P < 0.05) in birds fed 30% SPRM. Organ weights were similar across treatments except for gizzard which weighed highest (P < 0.05) in the control. For white meat; moisture, protein, fat, and ash were similar across treatments. For dark meat, moisture (P < 0.004) and fat (P < 0.03) were highest in the control, while protein and ash were similar among treatments. Birds fed the SPRM diets compared well with those fed the control for both performance and nutrient content of meat.

Maternal intake of eicosapentaenoic acid (EPA; 20:5 n-3) and docosahexaenoic acid (22:6 n-3) has been associated with reduced adiposity in children, suggesting the possibility to program adipose development through dietary fatty acids before birth. This study determined if enriching the maternal diet in fish oil, the primary source of EPA and DHA, affected adipose development in offspring. Broiler chickens were used because they are obesity-prone, and because fatty acids provided to the embryo can be manipulated through the hen diet. Hens were fed diets supplemented (2.8% wt:wt) with corn oil (CO; n-6) or fish oil (FO; n-3) for 28 d. Chicks from both maternal diet groups were fed the same diet after hatch. Maternal FO consumption enriched chick adipose tissue in EPA and DHA and reduced adiposity by promoting more, but smaller, adipocytes. This adipocyte profile was paralleled by lower expression of the adipogenic regulator PPARG and its co-activator PPARGC1B, and elevated expression of LPL. Proteomics identified 95 differentially abundant proteins between FO and CO adipose tissue, including components of glucose metabolism, lipid droplet trafficking, and cytoskeletal organization. These results demonstrate that the maternal dietary fatty acid profile programs offspring adipose development.

Epidemiologic studies associate perinatal intake of eicosapentaenoic acid (EPA, 20:5n–3) and docosahexaenoic acid (DHA, 22:6n–3) with reduced adiposity in children, suggesting that these fatty acids may alter adipose tissue development. The objective of this study was to determine whether enriching the perinatal diet in EPA and DHA reduces fat deposition in young chicks. Cobb 500 broiler chicks were fed isocaloric diets containing fat (8% wt:wt) from fish oil (FO), lard, canola oil, or flaxseed oil from 7 to 30 d of age. Adiposity (abdominal fat pad weight/body weight) at 30 d was not significantly affected by diet, but FO significantly reduced adipocyte size, increasing the abundance of small adipocytes. Plasma nonesterified fatty acid concentrations suggest that reduced adipocyte size was due, in part, to enhanced mobilization of fatty acids from adipose tissue. Our work indicates that dietary EPA and DHA effectively reduce the size of developing adipocytes in juveniles, which may limit adipose deposition and provide metabolic benefits.