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The diencephalic mRNA expression of NPYSR-Y5 (A), NPYSR-Y6 (B), and NPYSR-Y7 (C) in fasted chicks following i.c.v. injection of NPY (375 pmol) or saline under control thermoneutral temperature (CT: 30 AE 1°C) or a high ambient temperature (HT: 35 AE 1°C) for 1 h. Rectal temperatures (D) of chicks following i.c.v. injection of NPY (375 pmol), saline, or NPY (375 pmol) plus CGP71683 (3750 pmol) under CT for 1 h values are mean AE SEM for each group of 10-14 chicks in A-C and 8-10 chicks in D. Different letters indicate significant differences at P < 0.05 between groups.
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Exposure of chicks to a high ambient temperature (HT) has previously been shown to increase neuropeptide Y (NPY) mRNA expression in the brain. Furthermore , it was found that NPY has anti-stress functions in heat-exposed fasted chicks. The aim of the study was to reveal the role of central administration of NPY on thermotolerance ability and the in...
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... mRNA expression of NPYSRs-Y5, -Y6, and -Y7 significantly (P < 0.05) increased in the brain follow- ing NPY injection under both CT and HT ( Fig. 2A- C). HT also significantly (P < 0.05) increased NPYSR-Y6 mRNA expression (Fig. 2B). Figure 2D shows the effect of i.c.v. NPY and coinjection of CGP71683 plus NPY on rectal temperature under CT. The NPY-induced decreased rectal temperature was significantly (P < 0.05) attenuated by coinjection of CGP71683 plus NPY. Significance of time (P < ...
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... mRNA expression of NPYSRs-Y5, -Y6, and -Y7 significantly (P < 0.05) increased in the brain follow- ing NPY injection under both CT and HT ( Fig. 2A- C). HT also significantly (P < 0.05) increased NPYSR-Y6 mRNA expression (Fig. 2B). Figure 2D shows the effect of i.c.v. NPY and coinjection of CGP71683 plus NPY on rectal temperature under CT. The NPY-induced decreased rectal temperature was significantly (P < 0.05) attenuated by coinjection of CGP71683 plus NPY. Significance of time (P < 0.001) and interaction (P < 0.001) between treatment and time were found, ...
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... also significantly (P < 0.05) increased NPYSR-Y6 mRNA expression (Fig. 2B). Figure 2D shows the effect of i.c.v. NPY and coinjection of CGP71683 plus NPY on rectal temperature under CT. ...
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... NPYSR-Y5 was also found to slightly contribute to food intake in mammals ( Marsh et al. 1998). In this study, the mRNA expression of NPYSR-Y1 was not changed, but that of NPYSR-Y5 increased. Subse- quently, it was further confirmed that a coinjection of CGP71683 (an NPYSR-Y5 antagonist) plus NPY slightly attenuated the NPY-induced hypothermia (Fig. 2D), which suggests that NPYSR-Y5 is partially, but not entirely, involved with hypothermia. In addition, only NPYSR-Y6 was increased by heat stress, suggesting that HT has a strong influence on NPYSR-Y6. The function of NPYSRs-Y6 and -Y7 in chickens remains unknown. How- ever, until now, no antagonist has been available for NPYSRs-Y6 and ...
Citations
... In chickens, high ambient temperatures (HT) can cause increased brain neuropeptide Y (NPY) mRNA expression Tu et al., 2016), and central NPY injection attenuates heat stress responses Eltahan et al., 2017). Additionally, central injection of NPY is associated with reduced expression of heat-shock protein-70 and elevated glutathione synthase mRNA in the spleen, but not in the liver, in chicks, suggesting that central NPY may attenuate the splenic heat stress response . ...
... Male chicks were selected by feather identification at 2 days post-hatch and were used for the current study. Male chicks were used in this study because we always used male chicks in our previous studies related to heat challenge and NPY treatment Bahry et al., 2017;Eltahan et al., 2017). At 3 days of age, 2 chicks were housed in individual plastic cages (15 × 28 × 13 cm) for acclimatization for 24 h. ...
... Rectal temperature was measured using a digital thermometer with an accuracy of ±0.1 • C (Thermalert TH-5, Physitemp Instruments Inc., USA). The thermistor probe was inserted into the colon (rectum) through the cloaca to a depth of 2 cm as reported previously Chowdhury et al., 2015;Eltahan et al., 2017;Bahry et al., 2017;Nishimura et al., 2022). At the end of 3 h exposure to HT for both acute and chronic heat challenge, all chicks were immediately euthanized for culling by exposure to isoflurane (Mylan Inc., Tokyo, Japan). ...
High ambient temperatures (HT) can increase diencephalic neuropeptide Y (NPY) expression, and central injection of NPY attenuates heat stress responses while inducing an antioxidative state in the chick spleen. However, there is a lack of knowledge about NPY receptor expression, and its regulation by HT, in the chick spleen. In the current study, male chicks were used to measure the expression of NPY receptors in the spleen and other immune organs under acute (30 vs. 40 ± 1℃ for 3 h) or chronic (30 vs. 40 ± 1℃ for 3 h/day for 3 days) exposure to HT and in response to central injection of NPY (47 pmol, 188 pmol, or 1 nmol). We found that NPY-Y4 receptor mRNA was expressed in the spleen, but not in other immune organs studied. Immunofluorescence staining revealed that NPY-Y4 receptors were localized in the splenic pulp. Furthermore, NPY-Y4 receptor mRNA increased in the chick spleen under both acute and chronic exposure to HT. Central NPY at two dose levels (47 and 188 pmol) and a higher dose (1 nmol) did not increase splenic NPY-Y4 receptor mRNA expression or splenic epinephrine under HT (35 ± 1℃), and significantly increased 3-methoxy-4-hydroxyphenylglycol (MHPG) concentrations under HT (40 ± 1℃). In conclusion, increased expression of NPY-Y4 receptor mRNA in the spleen under HT suggests that Y4 receptor may play physiological roles in response to HT in male chicks.
... After being cleaned with 500 µL of ice-cold 70% ethanol, the DNA pellet was allowed to air dry and then suspended in 1 mL of Tris-EDTA buffer (pH 8.0), then kept at −30 • C until needed. The bacterial DNA from the cecum was examined for the expression of lactobacillus, Escherichia coli, and Clostridium perfringens by using real-time PCR according to the procedures previously described in Eltahan et al. [29]. Table 2 lists the primer sequences. ...
Simple Summary
This study investigated the impact of sucralose on rabbit intestine and caecal microbial activity, as well as various physiological parameters and performance indicators. One hundred and sixty 5-week-old rabbits were divided into four groups and administered different doses of sucralose. The results showed improved weight gain and feed conversion ratios in rabbits given sucralose, without significant effects on mortality. Sucralose altered blood parameters, decreasing glucose and triglyceride levels while increasing total lipids and cholesterol. It also influenced gut microbiota, increasing beneficial bacteria and decreasing harmful ones. The study suggests that caution should be taken in using sucralose, as it may have both positive and negative effects on rabbit health and gut microbiota.
Abstract
This study investigated how sucralose influenced rabbit intestine and caecal microbial activity, blood parameters, growth performance, carcass characteristics, and digestibility. In total, 160 5-week-old rabbits from the APRI line weighing 563.29 gm were randomly assigned to four experimental groups with four replicates—5 males and 5 females in each. Four experimental groups were used, as follows: SUC1, SUC2, and SUC3 got 75, 150, and 300 mg of sucralose/kg body weight in water daily, while the control group ate a basal diet without supplements. The results showed that both the control and SUC1 groups significantly (p < 0.05) increased daily weight gain and final body weight. Sucralose addition significantly improved feed conversion ratio (p < 0.05) and decreased daily feed intake (gm/d). The experimental groups do not significantly differ in terms of mortality. Furthermore, nutrient digestibility was not significantly affected by sucralose treatment, with the exception of crud protein digestion, which was significantly reduced (p < 0.05). Additionally, without altering liver or kidney function, sucralose administration dramatically (p < 0.05) decreased blood serum glucose and triglyceride levels while increasing total lipids, cholesterol, and malonaldehyde in comparison to the control group. Furthermore, the addition of sucrose resulted in a significant (p < 0.05) increase in the count of total bacteria, lactobacillus, and Clostridium spp., and a decrease in the count of Escherichia coli. Further analysis using 16S rRNA data revealed that sucralose upregulated the expression of lactobacillus genes but not that of Clostridium or E. Coli bacteria (p < 0.05). Therefore, it could be concluded that sucralose supplementation for rabbits modifies gut microbiota and boosts beneficial bacteria and feed conversion ratios without side effects. Moreover, sucralose could decrease blood glucose and intensify hypercholesterolemia and should be used with caution for human consumption.
... Commercial chickens for intensive meat and egg production are more sensitive to diseases due to a reduction in immune response throughout genetic selection improvement [1,2]. Heat stress harms all age groups of chickens, including young chicks [3], broilers of market age [4], and adult layers [5]. Several studies have demonstrated that heat stress negatively impacts feed intake, body weight, behaviours, egg production, eggshell quality, gut integrity, immunity, and mortality [6][7][8][9]. ...
... All primers were evaluated using routine PCR and gel electrophoresis before real-time PCR (TaKaRa PCR Thermal Cycler Dices, Takara, Shiga, Japan). The expression of chicken IL-2 and IFN-γ in the PBMC were quantified with real-time PCR following the steps that are written elsewhere in Eltahan et al. [3]. The primer sequences are presented in Table 2. Relative mRNA expressions have been calculated by comparing the thermal cycles needed to generate threshold amounts of product (PCR-ct). ...
Simple Summary
The current study shows that using cold water under high ambient temperature (CW: 15 ± 1 °C; HT: HT: 35 ± 1 °C) in heat-exposed laying hens is capable of maintaining productive efficiency and immune-suppressing under heat stress. The feed intake and egg production were enhanced after using the cold water under heat stress. Moreover, the cold water restored the decline in the level of B-cell, helper T cells, and the ratio of helper/cytotoxic T cells in peripheral blood mononuclear cells, as well as the concentration of IL-2, IFN-γ, and immunoglobulin G in plasma. Therefore, cold water is one of the mechanisms that can be considered under heat stress.
Abstract
This study aimed to investigate the effects of cold drinking water on cellular and humoral immunity in heat-exposed laying hens. One hundred and eight laying hens at 19 weeks old were placed into three treatments with six replicates of six hens in each group as follows: (1) hens were provided with normal drinking water (NW) under the control of thermoneutral temperature (CT: 25 ± 1 °C; CT + NW), (2) hens were provided with NW under high ambient temperature (HT: 35 ± 1 °C; HT + NW) for 8 h/d for a month, and (3) hens were treated under HT with cold drinking water (CW: 15 ± 1 °C; HT + CW) for 8 h/d for a 4-weeks. Then, the feed consumption, egg production, egg weight, feed conversion ratio, and blood immune parameters were investigated. The results showed that cold drinking water (CW) caused a significant (p < 0.05) recovery in the reduction of food intake and egg production due to heat stress; however, there was no significant effect (p > 0.05) on egg weight and feed conversion ratio. Moreover, CW significantly (p < 0.05) restored the immune-suppressing effects of heat stress on the contents of peripheral blood mononuclear cells, including B-cell (BU-Ia), helper T cell (CD4), and the ratio of helper/cytotoxic T cell (CD4/CD8). In addition, CW significantly (p < 0.05) recovered the reduction on the level of mRNA expression of interleukin-2 (IL-2) and interferon-gamma (IFN-γ), as well as significantly (p < 0.05) restored the reduction of plasma concentration of IL-2, IFN-γ and immunoglobulin G in heat-stressed laying hens. These results prove that CW increased heat dissipation and enhanced feed intake, egg production, and cellular and humoral immunity in heat-exposed laying hens.
... To quantify the expression of chicken IL-2 mRNA, real-time quantitative PCR was conducted using laStratagene MX 3000P (Agilent Technologies, Santa Clara, CA, USA) with denaturation step at 95°C for 30 s, then 40 cycles of amplification at 95 °C for 5 s and a primer-specific annealing/extension temperature for 30 s. Relative mRNA expression was calculated by comparing the number of thermal cycles required to generate threshold amounts of product (PCR-ct). PCR-ct was calculated for chicken IL-2 and normalized to the expression RNA polymerase-II (RP-II) (Eltahan et al., 2017); we confirmed that RP-II expression was not altered under our experimental conditions. IL-2 mRNA expression was calculated as 2 -ΔΔ PCR-ct , as previously described (Schmittgen and Livak, 2008). ...
Silicate minerals are common additives in poultry feed. To assess their effects, we added zeolite (ZEO) and methyl-sulfonyl-methane (MSM) to broiler chicken diets. A total of 960 one-day-old Ross broiler chicks were randomly divided into four dietary groups with six replicates. Each broiler was maintained until it reached 35 days of age. A completely randomized 2 × 2 experimental design was used, with two ZEO (0 and 1.0%) and two MSM (0 and 0.10%) levels. We observed an additive effect (P<0.05) on interleukin-2 (IL-2) concentrations in broiler bursa and serum when both ZEO and MSM were present. Both ZEO or MSM produced significant (P<0.05) increases in body weight, weight gain, and feed intake. Both increased IL-2 and IL-6 levels in the bursa and serum. Neither affected the serum concentrations of albumin, AST, cholesterol, HDL cholesterol, glucose, total protein, or triglycerides. In summary, these results support supplementation with ZEO and MSM in broiler diets, both separately and in combination.
... The proportional increase in brain ornithine levels following central administration of its precursor l-arginine was found to be accompanied by alterations in amino acid concentrations in the chick brain (Suenaga et al., 2008). In addition, previous studies have reported the influence of NPY on both central and peripheral amino acid metabolism (Eltahan et al., 2017;Tran et al., 2021). Therefore, the aim of the current study was to examine the involvement of ornithine signaling pathway in the orexigenic effect induced by NPY by determining food intake after direct central co-injection of NPY and ornithine, and investigating the involvement of free amino acid metabolism in the central and peripheral systems of chicks. ...
Ornithine has been identified as a potential satiety signal in the brains of neonatal chicks. We hypothesized that brain nutrient signals such as amino acids and appetite-related neuropeptides synergistically regulate food intake. To test this hypothesis, we investigated the interaction between neuropeptide Y (NPY) and ornithine in the control of feeding behavior in chicks and the associated central and peripheral amino acid metabolic processes. Five-day-old chicks were intracerebroventricularly injected with saline, NPY (375 pmol), or NPY plus ornithine (2 or 4 μmol) at 10 μl per chick, and then subjected to ad libitum feeding conditions; food intake was monitored for 30 min after injection. Brain and plasma samples were collected after the experiment to determine free amino acid concentrations. Co-injection of NPY and ornithine significantly attenuated the orexigenic effect induced by NPY in a dose-dependent manner. Central NPY significantly decreased amino adipic acid, asparagine, γ-aminobutyric acid, leucine, phenylalanine, tyrosine, and isoleucine levels, but significantly increased lysine levels in the brain. Co-injection of NPY and ornithine significantly increased ornithine and proline levels in all examined brain regions, but decreased diencephalic tryptophan and glycine levels compared with those of the control and NPY-alone groups. Co-injection of NPY and high-dose ornithine significantly decreased methionine levels in all brain regions. Central NPY significantly suppressed the plasma concentrations of amino acids, including proline, asparagine, methionine, phenylalanine, tyrosine, leucine, isoleucine, glycine, glutamine, alanine, arginine, and valine, and this reduction was greater when NPY was co-injected with ornithine. These results suggest that brain ornithine interacts with NPY to regulate food intake in neonatal chicks. Furthermore, central NPY may induce an anabolic effect that is modified by co-injection with ornithine.
... Early exposure to elevated temperatures helps birds adapt to heat later in life [106][107][108]. Initially, it was thought that brooding chicks did not experience stress from elevated temperatures, but it is now recognized that chicks are sensitive to heat stress [106,[109][110][111]. The temperature that was selected in the current study (i.e., 36 • C) would be expected to elicit a thermal stress response in Ross 308 broilers during brooding as chicks as young as 7 days-of-age experience heat stress [112], and thermal stress after brooding occurs at 27 • C [113]. ...
The impact of physiological stress on the metabolome of breast muscle, liver, kidney, and hippocampus was investigated in Ross 308 broiler chicks. Simulated on-farm stressors were compared to a corticosterone model of physiological stress. The three different stressors investigated were: (i) corticosterone at a dose of 15 mg/kg of feed; (ii) heat treatment of 36 °C and 40% RH for 8 h per day; and (iii) isolation for 1 h per day. Liver, kidney, breast muscle, and hippocampus samples were taken after 2, 4, 6, and 8 days of stress treatment, and subjected to untargeted 1H-nuclear magnetic resonance (NMR) spectroscopy-based metabolomic analysis to provide insights on how stress can modulate metabolite profiles and biomarker discovery. Many of the metabolites that were significantly altered in tissues were amino acids, with glycine and alanine showing promise as candidate biomarkers of stress. Corticosterone was shown to significantly alter alanine, aspartate, and glutamate metabolism in the liver, breast, and hippocampus, while isolation altered the same pathways, but only in the kidneys and hippocampus. Isolation also significantly altered the glycine, serine, and threonine metabolism pathway in the liver and breast, while the same pathway was significantly altered by heat in the liver, kidneys, and hippocampus. The study’s findings support corticosterone as a model of stress. Moreover, a number of potential metabolite biomarkers were identified in chicken tissues, which may allow producers to effectively monitor stress and to objectively develop and evaluate on-farm mitigations, including practices that reduce stress and enhance bird health.
... The first aim of the current study was to examine the effect of central NPY on changes in HSP-70 and GSS mRNA expression in the spleen and liver in heat-exposed chicks. Plasma biochemical profiles can indicate the extent of heat stress in chicks [24], and central injections of NPY can reduce plasma glucose and triacylglycerol concentrations in chicks [25]. It was further reported that plasma glucose [26] and plasma uric acid [27] levels were increased by exposure to HT in broilers. ...
... NPY (Porcine, Peptide Institute, Osaka, Japan) was dissolved in a vehicle of 0.85% saline containing 0.1% Evans Blue (Wako Pure Chemical Industries, Ltd., Osaka, Japan). We used porcine NPY because Lundell et al. [31] reported that this peptide showed affinity to chicken NPY Y1, Y4 and Y5 receptors, and we had used porcine NPY for our previous heat stress studies in chicks [25,32]. Evans Blue saline solution was used for the control group, as in previous studies [33,34]. ...
... Chicks were fed ad libitum until ICV injection was performed. On the day of the experiment, chicks (n = 12 per group) were intracerebroventricularly injected with 10 μL of either 0 or 375 pmol NPY, based on our previous reports showing that 375 pmol was an effective dose of NPY to regulate rectal temperature [25,32,33]. Chicks were returned to their cages and placed in a temperature-controlled chamber (Panasonic Electric Co. Ltd., Japan; Catalog number: Panasonic MIR-254) under fasting conditions and maintained at either HT (35 ± 1 • C) for the heat stress challenge or CT (30 ± 1 • C) for 1 h. ...
Previously it was found that mRNA expression of neuropeptide Y (NPY) was increased in the chicken brain under heat stress. NPY has also been reported as an anti-stress factor to regulate brain functions in heat exposed chicks. However, to the best of our knowledge, there is no report on the action of central NPY in the immune organs under heat stress. The aim of this study was to examine whether central injection of NPY can regulate heat stress response in the spleen and liver. After intracerebroventricular (ICV) injection of NPY, chicks were exposed to control thermoneutral temperature (CT: 30 ± 1°C) or high ambient temperature (HT: 35 ± 1°C) chambers for 60 min. Central injection of NPY caused lowering in rectal temperature under CT, but not under HT. Moreover, ICV injection of NPY caused a significant lower mRNA expression of heat-shock protein-70 and higher expression of glutathione synthase in the spleen, but not liver. Furthermore, plasma uric acid concentrations were significantly increased by the ICV injection of NPY in chicks under HT. These results indicate that brain NPY may contribute to attenuate the intracellular heat stress response and enhance antioxidative status in the immune organ, spleen in chicks.
... Additionally, the NPYergic system has been associated with behavioral resilience to psychological stress (PSS) in rats [75]. A decrease in rectal temperature along with increment in HSP-70 expression were noted in chicks that were exposed to HS and centrally administrated with NPY, indicating a thermoregulatory role of NPY during thermal stress [76]. Unlike the results obtained in this study, NPY mRNA expression was significantly increased in the hypothalamus of chicks [77] and rats [78] in response to an acute HS or restraint stress, respectively. ...
Exposure to high ambient temperature is a stressor that influences both biological and behavioral functions and has been previously shown to have an extensive impact on brain structure and function. Physiological, cellular and behavioral responses to heat-stress (HS) (40–41 °C, 2 h) were evaluated in adult male Sprague-Dawley rats. The effect of HS exposure before predator-scent stress (PSS) exposure (i.e., HS preconditioning) was examined. Finally, a possible mechanism of HS-preconditioning to PSS was investigated. Immunohistochemical analyses of chosen cellular markers were performed in the hippocampus and in the hypothalamic paraventricular nucleus (PVN). Plasma corticosterone levels were evaluated, and the behavioral assessment included the elevated plus-maze (EPM) and the acoustic startle response (ASR) paradigms. Endogenous levels of heat shock protein (HSP)-70 were manipulated using an amino acid (L-glutamine) and a pharmacological agent (Doxazosin). A single exposure to an acute HS resulted in decreased body mass (BM), increased body temperature and increased corticosterone levels. Additionally, extensive cellular, but not behavioral changes were noted. HS-preconditioning provided behavioral resiliency to anxiety-like behavior associated with PSS, possibly through the induction of HSP-70. Targeting of HSP-70 is an attractive strategy for stress-related psychopathology treatment.
... Of particular importance in chicken is the interaction between NPY and heat stress. Indeed, NPY has been shown to induce hypothermia in birds [129,130], and is known to be modulated by heat stress in birds [131]. As this state also induces inflammation, further study of the role of NPY and its interaction with the immune system during this critical physiological state may provide future insights into helping the poultry industry manage heat stress. ...
Neuropeptide Y (NPY) is one of the most abundant and ubiquitously expressed neuropeptides in both the central and peripheral nervous systems, and its regulatory effects on feed intake and appetite- have been extensively studied in a wide variety of animals, including mammalian and non-mammalian species. Indeed, NPY has been shown to be involved in the regulation of feed intake and energy homeostasis by exerting stimulatory effects on appetite and feeding behavior in several species including chickens, rabbits, rats and mouse. More recent studies have shown that this neuropeptide and its receptors are expressed in various peripheral tissues, including the thyroid, heart, spleen, adrenal glands, white adipose tissue, muscle and bone. Although well researched centrally, studies investigating the distribution and function of peripherally expressed NPY in avian (non-mammalian vertebrates) species are very limited. Thus, peripherally expressed NPY merits more consideration and further in-depth exploration to fully elucidate its functions, especially in non-mammalian species. The aim of the current review is to provide an integrated synopsis of both centrally and peripherally expressed NPY, with a special focus on the distribution and function of the latter.
... This suggests that the POA responds to HAT by inducing sleep to reduce metabolic heat production and may stimulate pathways associated with heat loss in mammals. PGD2 is also associated with an increase in neuropeptide Y (NPY) secretion in mice [81], a neuropeptide which is known to induce hypothermia in birds [82][83][84]. However, the role of PGD2 in avian sleep and thermoregulation has yet to be assessed. ...
... Similarly, broiler chicks injected with NPY via intracerebroventricular (ICV) injection during heat exposure had a diminished orexigenic response to the NPY [87], while layer-type chicks ICV injected with NPY during heat exposure responded similarly to thermoneutral chicks [82]. NPY treatment reduced body temperature in layer-type chickens [82][83][84], however this has yet to be explored in broilers. These data collectively suggest that the hypothermic effect of NPY may not be present in broilers. ...
Simple Summary
Heat stress is a major environmental condition negatively impacting the wellbeing of various avian species. In chickens, heat exposure is associated with disruption of metabolic and immune system function, and an increased risk of mortality. This has a negative impact on the food economy, as chicken products make up roughly 34% of the world’s protein. Techniques to mitigate exposure to high temperatures have been discussed in depth, and most research suggests that the root cause of heat stress-induced physiological aberrations is alterations in the stress response and reduced food intake. Unfortunately, little is known about thermoregulation in birds. That thermoregulation, food intake, and the stress response are all mediated by the hypothalamus make it tempting to speculate that it is the central hub at which these systems interact and signals from diverse pathways are integrated. Thus, this review discusses the neural circuitry in birds associated with thermoregulation, food intake, and stress response at the level of the hypothalamus, with a focus on how these systems might interact in the presence of heat exposure.
Abstract
Heat stress is one of the major environmental conditions causing significant losses in the poultry industry and having negative impacts on the world’s food economy. Heat exposure causes several physiological impairments in birds, including oxidative stress, weight loss, immunosuppression, and dysregulated metabolism. Collectively, these lead not only to decreased production in the meat industry, but also decreases in the number of eggs laid by 20%, and overall loss due to mortality during housing and transit. Mitigation techniques have been discussed in depth, and include changes in air flow and dietary composition, improved building insulation, use of air cooling in livestock buildings (fogging systems, evaporation panels), and genetic alterations. Most commonly observed during heat exposure are reduced food intake and an increase in the stress response. However, very little has been explored regarding heat exposure, food intake and stress, and how the neural circuitry responsible for sensing temperatures mediate these responses. That thermoregulation, food intake, and the stress response are primarily mediated by the hypothalamus make it reasonable to assume that it is the central hub at which these systems interact and coordinately regulate downstream changes in metabolism. Thus, this review discusses the neural circuitry in birds associated with thermoregulation, food intake, and stress response at the level of the hypothalamus, with a focus on how these systems might interact in the presence of heat exposure.
