High ambient temperatures are a critical challenge in the poultry industry which is a key producer of the animal-based food. To evaluate heat stress levels, various parameters have been used, including growth rates, blood metabolites, and hormones. The most recent advances have explored expression profiling of genes that may play vital roles under stress. A high ambient temperature adversely affects nutrient uptake and is known to modulate the expression of genes encoding for sodium-dependent glucose transporters, glucose transporters, excitatory amino acid transporters, and fatty acid-binding proteins which are responsible for the absorption of macronutrients in the intestine. Various defensive activities are stimulated to protect the cell of different tissues from the heat-generated stress, including expression of early stress response genes coding for heat shock protein (HSP), c-FOS like protein, brain-derived neurotrophic factor (BDNF), and neuronal nitric oxide synthase (nNOS); antioxidant enzyme genes such as superoxide dismutase (SOD), catalase (CAT), and nicotinamide adenine dinucleotide phosphate oxidase (NOX4); and immune-related genes such as cytokines and toll-like receptors (TLRs). The potential role of HSPs in protecting the cell from stress and their presence in several tissues make them suitable markers to be evaluated under heat stress. BDNF and c-FOS genes expressed in the hypothalamus help cells to adapt to an adverse environment. Heat causes damage to the cell by generating reactive oxygen species (ROS). The NOX4 gene is the inducer of ROS under heat stress, which is in turns controlled by antioxidant enzymes such as SOD and CAT. TLRs are responsible for protecting against pathogenic attacks arising from enhanced membrane permeability, and cytokines help in controlling the pathogen and maintaining homeostasis. Thus, the evaluation of nutrient transporters and defense mechanisms using the latest molecular biology tools has made it possible to shed light on the complex cellular mechanism of heat-stressed chickens. As the impacts of heat stress on the above-mentioned aspects are beyond the extent to which the reduced growth performance could be explained, heat stress has more specific effects on the regulation of these genes than previously thought.Graphical Effect of heat exposure on the nutrient transporters, antioxidants, and immune inflammation in chickens. Most of the nutrient transporters were suppressed under heat stress. Increase in the production of reactive oxygen species resulted in enhanced production of antioxidant enzymes. Expression of various proinflammatory cytokines and toll-like receptors were enhanced due to heat stress in chicken.

This study was conducted to evaluate the effects of temperature-humidity index (THI) on the mortality and the panting rates in hens exposed to varying thermal environments. Hens were challenged with an acute elevation in THI in Experiment 1, where dry-bulb temperature and relative humidity were set at ~27°C and 56% at the beginning of the experiment and changed to 36°C and 45% at its conclusion, respectively. In Experiment 2, different groups of hens were exposed to a progressive increase in THI, with similar ranges to those used in the previous experiment. In Experiment 3, the hens used in Experiment 2 were again challenged by THI conditions, the intensity of which ranged between those used in the previous two experiments. In Experiment 4, panting rates were recorded under varying THI. In the last, plasma biochemical profiles were determined in blood taken from hens subjected to experimental conditions similar to those in Experiment 2. When THI was acutely elevated from 24.2° to 32.1°C within 1 h and then maintained over 4.5 h, no mortality was detected in the first hour, but exceeded 95% after 5 h, and reached 100% at 5.5 h. A gradual increase in THI to 31.2°C over 6 h did not result in mortality during the first 3 h. When THI was set below the conditions in Experiment 1 but above those in Experiment 2, mortality was 29% at 4 h, 75% at 5 h, and 79% at 8 h. However, no mortality was detected in their respective control groups. Panting was not observed under 25.3°C and was largely variable under 30°C. However, all hens exhibited panting exceeding 250 counts/min and 60% mortality at 34°C when heat stress continued for a duration of up to 280 min. In Experiment 5, high ambient THI resulted in significant reductions in plasma albumin, amylase and aspartate aminotransferase, compared with those in control group (P < 0.05). These results suggest that an acute elevation of THI has more severe effects on mortality in hens than gradual changes even when temperature and humidity are similar in both cases.

The objective of this study was to investigate the effects of dietary corticosterone on egg quality. For 2 weeks hens received either control or experimental diet containing corticosterone at 30 mg/kg diet. Feed intake and egg production were monitored daily, and body weight measured weekly. Egg weights and egg quality were measured daily. Corticosterone treatment resulted in a remarkable increase in feed intake and sharp decrease in egg production compared with control (p<0.05) whereas body weight remained unchanged. Decreased albumen height, but no changes in egg weight, led to decreased Haugh unit (p<0.05). Corticosterone caused elevated eggshell thickness (p<0.05) without altering weight and strength, suggesting possible changes in shell structure. Yolk color and redness were increased by corticosterone (p<0.05) but lightness and yellowness were either not changed or inconsistent over the time period of measurements. Increased concentrations in plasma were also found for corticosterone, glucose, cholesterol, creatinine, uric acid, albumin, aspartate aminotransferase, creatine kinase, lactate dehydrogenase, total protein, and amylase (p<0.05), suggesting that corticosterone increased protein breakdown, renal dysfunctions and pancreatitis. Together, the current results imply that dietary corticosterone affects egg quality such as yolk colors and shell thickness, in addition to its effects on feed intake and egg production.

In avian species, heat stress (HS) is usually the result of being exposed to high ambient temperatures, whereas oxidative stress (OS) results from the overproduction of reactive oxygen species. The current literature suggests that HS often leads to OS. Therefore, this systematic review and meta-analysis was conducted to assess the effects of dietary supplementation of glutamine on the antioxidant status and growth performances in heat-stressed broilers. A total of 13 studies were deemed eligible after an exhaustive search of the literature from Google Scholar, PubMed, and Scopus. Briefly, the following criteria were used to select the studies: trials performed on broilers; publication in peer-review journals using English as the text language; and sufficient details about the design and inclusion of dietary glutamine as a treatment for HS. Two main categories of outcomes were extracted from the studies included in the review: growth parameters and OS markers. For the meta-analysis, a random effect model was used when the heterogeneity was higher than 50%, and a fixed effect model was applied otherwise. Pooled standardized mean differences (SMD), and mean differences (MD) with their confidence intervals (CI) from the studies revealed that dietary glutamine could increase body weight gain (SMD = 0.70, CI = 0.50 to 0.90, p < 0.05), and feed intake (FI) (SMD = 0.64, CI = 0.43 to 0.86, p < 0.05), and reduce the feed conversion ratio (MD = −0.05, CI = −0.07 to −0.02, p < 0.05) in heat-exposed birds. Additionally, higher glutamine (SMD = 1.21, CI = 1.00 to 1.43, p < 0.05), glutathione (SMD = 1.25, CI = 0.88 to 1.62, p < 0.05), superoxide dismutase (SOD) (SMD = 0.97, CI = 0.58 to 1.36, p < 0.05), and catalase (SMD = 0.94, CI = 0.72 to 1.16, p < 0.05) levels were recorded in the serum, breast, and thigh muscle after supplementation of glutamine. Furthermore, the subgroup analysis revealed that malondialdehydes levels were decreased only in the serum (SMD = −0.83, CI = −1.25 to −0.41, p < 0.001) and thigh muscle (SMD = −1.30, CI = −1.86 to −0.35, p < 0.001) while glutathione peroxidase (GPX) activity was increased in the breast (SMD = 1.32, CI = 0.95 to 1.68, p < 0.05) and thigh muscle (SMD = 1.53, CI = 1.06 to 1.99, p < 0.05). Meta-regression models indicated that longer periods of heat exposure were inversely associated with the effectiveness of dietary glutamine in increasing FI, GPX, and SOD (p < 0.05). Besides, increasing the dietary concentration of glutamine led to higher GPX and SOD levels (p < 0.05). Taken together, results suggest that dietary supplementation of glutamine can effectively mitigate the deleterious effects of HS by enhancing the antioxidant status and increasing growth performances in broilers.

The aim of this study was to explore the outcomes of an in ovo GABA injection in broilers challenged with HS. In Experiment 1, 210 Arbor Acres eggs were allocated to five treatments: no-injection, and in ovo injection of 0.6 mL of 0%, 5%, 10%, or 20% of GABA. Hatchling weight and CWEWR were significantly increased in the 5% GABA group. In ovo, injection of 10% GABA solution caused a significant decrease in plasma cholesterol and increased plasma total antioxidant capacity of hatchlings. Experiment 2 was conducted with 126 fertile Arbor Acres eggs distributed into one of two groups. At 17.5 days of incubation, one received no injection, and the other was fed 0.6 mL of 10% GABA. On day 10, one subgroup (4 replicates * 3 birds) from each treatment was submitted to HS (38 ± 1 °C for 3 h) while the other was kept at a thermoneutral temperature (29 ± 1 °C). An in ovo injection of GABA significantly increased total antioxidant capacity, but reduced malondialdehyde levels, hepatic mRNA levels of HSP70, FAS, and L-FABP with HS. In conclusion, an in ovo GABA injection improves CWEWR and antioxidant status at hatch, and enhances antioxidant status while downregulating the expression of HSP70 and fatty acid metabolism-related genes in young chicks under HS.

Healthy chickens are necessary to meet the ever-increasing demand for poultry meat. Birds are subjected to numerous stressful conditions under commercial rearing systems, including variations in the environmental temperature. However, it is difficult to counter the effects of global warming on the livestock industry. High environmental temperature is a stressful condition that has detrimental effects on growth and production performance, resulting in decreased feed intake, retarded growth, compromised gut health, enhanced oxidative stress, and altered immune responses. Traditional approaches include nutritional modification and housing management to mitigate the harmful effects of hot environments. Currently, broiler chickens are more susceptible to heat stress (HS) than layer chickens because of their high muscle mass and metabolic rate. In this review, we explored the possibility of in ovo manipulation to combat HS in broiler chickens. Given their short lifespan from hatching to market age, embryonic life is thought to be one of the critical periods for achieving these objectives. Chicken embryos can be modulated through either temperature treatment or nourishment to improve thermal tolerance during the rearing phase. We first provided a brief overview of the harmful effects of HS on poultry. An in-depth evaluation was then presented for in ovo feeding and thermal manipulation as emerging strategies to combat the negative effects of HS. Finally, we evaluated a combination of the two methods using the available data. Taken together, these investigations suggest that embryonic manipulation has the potential to confer heat resistance in chickens.