Exogenous nutrients are essential for body and skeletal muscle growth in newly hatched chicks, and delaying post-hatch feeding negatively affects body growth, meat yield, and meat quality. The aim of this study was to investigate the effects of delayed post-hatch feeding on the metabolic profiles of broiler chickens using a combination of targeted and untargeted metabolomics. Newly hatched chicks had either immediate free access to feed (freely fed chicks) or no access to feed from 0 to 2 days of age (delayed-fed chicks); both groups were subsequently provided feed ad libitum until 13 days of age. Untargeted metabolomic analysis was performed using gas chromatography-mass spectrometry, whereas targeted metabolomic analysis of amino acids was performed using high-performance liquid chromatography with ortho-phthalaldehyde derivatization. Delayed feeding increased the plasma levels of sucrose, maltose, serotonin, lactitol, gentiobiose, xylitol, threonic acid, and asparagine, and decreased the plasma levels of creatinine, aspartic acid, and glutamic acid. In addition, the digestibility of the nitrogen-free extract (starch and sugar) and the cecal butyric acid concentration increased in chicks subjected to delayed feeding. In contrast, delayed feeding did not affect muscle protein degradation or digestibility in chicks. Taken together, our results indicate that delaying feeding until 48 h post-hatch alters multiple metabolic pathways, which are accompanied by changes in intestinal carbohydrate digestion and cecal butyric acid content in broiler chickens.

Brain amino acid metabolism has been reported to regulate body temperature, feeding behavior and stress response. Central injection of taurine induced hypothermic and anorexigenic effects in chicks. However, it is still unknown how the amino acid metabolism is influenced by the central injection of taurine. Therefore, the objective of this study was to investigate the changes in brain and plasma free amino acids following central injection of taurine. Five-day-old male Julia layer chicks (n = 10) were subjected to intracerebroventricular (ICV) injection with saline or taurine (5 µmol/10 µL). Central taurine increased tryptophan concentrations in the diencephalon, and decreased tyrosine in the diencephalon, brainstem, cerebellum, telencephalon and plasma at 30 min post-injection. Taurine was increased in all the brain parts after ICV taurine. Although histidine and cystathionine concentrations were increased in the diencephalon and brainstem, several amino acids such as isoleucine, arginine, methionine, phenylalanine, glutamic acid, asparagine, proline, and alanine were reduced following central injection of taurine. All amino acid concentrations were decreased in the plasma after ICV taurine. In conclusion, central taurine quickly changes free amino acid concentrations in the brain and plasma, which may have a role in thermoregulation, food intake and stress response in chicks.

Higher or lower incubation temperature may impose some degree of stress on developing poultry embryos. This study was designed to delineate the effects of prenatal thermal stress on serum levels of acute-phase proteins (APPs), namely ceruloplasmin (CPN) and alpha-1-acid glycoprotein (AGP), the regulation of brain mRNA levels of heat shock protein (Hsp) 70, and serum levels of corticosterone (CORT) in embryos and neonatal chicks. Hatching eggs were subjected to three thermal treatments; (i) standard optimum temperature throughout (SS: 37.8 °C and 56 % RH), (ii) heat stress for 12 h daily (HS: 40.0 °C and 56 % RH), and (iii) cold stress for 12 h daily 18 (CS: 30.2 °C and 56 % RH). The heat and cold stress treatments were imposed from the 10th to the 18th day of incubation (ED). Results showed that thermal stress had a negligible effect on hatchability rate and body temperatures of neonatal chicks. The CS treatment was detrimental to embryonic growth. The HS treatment elevated AGP (ED 16, ED 18, and post-hatch day 1), CPN (on post-hatch day 1), and CORT (ED 14). On the contrary, the CS embryos had reduced AGP (ED14, ED16, ED18, and post-hatch day 1), CPN (ED 16), and CORT (ED 14, ED 16, ED 18). The brain mRNA levels of Hsp70 were upregulated throughout the experimental period in both the HS and CS embryos and chicks. Based on these modifications, AGP, together with Hsp70 mRNA expression, could be considered effective biomarkers useful to evaluate the magnitude and the time response of embryos and neonatal chicks to prenatal thermal stress. It is concluded that developing chicken embryos have the ability to evoke APPs, Hsp70 and CORT reactions which are important to cope with thermal stress.

Brain monoamines are reported to regulate body temperature and food intake. The objective of this study was to investigate the mechanism of brain monoamine metabolism in taurine-induced hypothermia and appetite suppression. In Experiment 1, 5-day-old male Julia layer chicks (n = 10) were subjected to intracerebroventricular (ICV) injection with saline or taurine (5 μmol/10 μL). In Experiment 2, the chicks were ICV injected with saline, taurine, fusaric acid (dopamine-β-hydroxylase inhibitor: 558 nmol), or taurine with fusaric acid. In Experiment 3, the chicks were ICV injected with saline, taurine, para-chlorophenylalanine (PCPA, tryptophan hydroxylase inhibitor: 400 nmol), or taurine with PCPA. In Experiment 4, the chicks were ICV injected with saline, taurine, clorgyline (monoamine oxidase inhibitor: 81 nmol), or taurine with clorgyline. Central taurine lowered rectal temperature at 30 min post-injection and increased norepinephrine in the brainstem and its metabolite 3-methoxy-4-hydroxyphenylglycol in both the diencephalon and brainstem. Similarly, taurine treatment induced increases in serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid in the diencephalon. Fusaric acid completely and PCPA partially, but not clorgyline, attenuated taurine-induced hypothermia. The anorexigenic effect of taurine was partially attenuated by PCPA, but not fusaric acid nor clorgyline. In conclusion, central taurine activates dopamine-β-hydroxylase and tryptophan hydroxylase to produce norepinephrine and 5-HT, and then induces hypothermia, but 5-HT alone may be linked with taurine-induced anorexia in chicks.

The aim of this study was to examine the central action of taurine on body temperature and food intake in neonatal chicks under control thermoneutral temperature (CT) and high ambient temperature (HT). Intracerebroventricular injection of taurine caused dose-dependent hypothermia and reduced food intake under CT. The mRNA expression of the GABAA receptors, GABAAR-α1 and GABAAR-γ, but not that of GABABR, significantly decreased in the diencephalon after central injection of taurine. Subsequently, we found that picrotoxin, a GABAAR antagonist, attenuated taurine-induced hypothermia. Central taurine significantly decreased the brain concentrations of 3-methoxy-4-hydroxyphenylglycol, a major metabolite of norepinephrine; however, the concentrations of serotonin, dopamine, and the epinephrine metabolites, 3,4-hydroxyindoleacetic acid and homovanillic acid, were unchanged. Although hypothermia was not observed under HT after central injection of taurine, plasma glucose and uric acid levels were higher, and plasma sodium and calcium levels were lower, than those in chicks under CT. In conclusion, brain taurine may play a role in regulating body temperature and food intake in chicks through GABAAR. The changes in plasma metabolites under heat stress suggest that brain taurine may play an important role in maintaining homeostasis in chicks.

Excessive lipid peroxidation negatively affects the physiological response and meat quality of chickens. Delaying post-hatch feeding was previously found to increase lipid peroxidation in the skeletal muscle of finishing broiler chickens. The aims of this study were to investigate the effects of delayed post-hatch feeding on lipid peroxidation and the mRNA expressions of antioxidant enzymes in the pectoralis major muscle of broiler chicks during the post-hatching period. Newly hatched chicks either had immediate free access to feed (freely-fed chicks) or had no access to feed from 0 to 2 days old (delayed-fed chicks), after which both groups were fed ad libitum until 4 or 13 days old. The lipid peroxidation level was higher in the delayed-fed than freely-fed chicks at 2, 4, and 13 days old. At 2 days old, the mRNA expressions of Cu/Zn-SOD, Mn-SOD, and GPX7 were lower in the delayed-fed than freely-fed chicks, while catalase mRNA levels did not differ. Furthermore, at 4 and 13 days old, lower mRNA expressions of Cu/Zn-SOD and Mn-SOD were observed in the delayed-fed than freely-fed chicks. These results suggest that delaying post-hatch feeding reduces the mRNA levels of Cu/Zn-SOD and Mn-SOD, consequently affecting muscle lipid peroxidation in chicks during subsequent growth.

Animals at the neonatal stage have to eat more to support better growth and health. However, it is difficult to understand the mechanism of feeding during an early stage of life in the brain of the rodent model. Chickens are precocial and they can look for their food by themselves right after hatching. Neonatal chicks have a relatively large-sized brain; therefore, the drugs are easy to administer centrally and changes in food intake can be clearly monitored. Sleeping status, which affects food intake, can be estimated from the posture. The closest vertebrate outgroup to mammals is birds, but it was reported that the organization of the human genome is closer to that of the chicken than the mouse. Thus, it is important to understand the central mechanism of feeding regulation in the neonatal chicks. In neuropeptides, the number of candidates as the orexigenic factor was less than those as the anorexigenic factor, even at an early growth stage. Some of the neuropeptides have reverse effects, e.g., ghrelin and prolactin releasing peptides, or no effects compared to the effects confirmed in mammals. Some of the genetic differences between meat-type (broiler) and layer-type chickens would explain the difference in food intake. On the other hand, it was difficult to explain the feeding mechanism by neuropeptides alone, as neonatal chicks have a repeated feeding, sleeping, and resting behavior within a short period. Some of the amino acids and their metabolites act centrally to regulate feeding with sedative and hypnotic effects. In conclusion, endogenous neuropeptides and endogenous and/or exogenous nutrients like amino acids collaborate to regulate feeding behavior in neonatal chicks.

This study was conducted to analyse the effects of leucine (Leu) and glycine (Gly)-Leu peptide on expressions of key signalling molecules in mTOR pathway of skeletal muscle satellite cells in neonatal chicks. The 4-day-old male AA broilers with similar weight were selected to obtain the broiler skeletal muscle satellite cells with the two-step method of collagenase-I and trypsin digestion. The satellite cells were subjected to primary culture in vitro, and they were cultured in DMEM medium with the Leu concentration of 0.2 mM and 2 mM as well as with the Gly-Leu peptide concentration of 0.2 mM and 2 mM. The experiment lasted for 5 days. The results showed that TOR, S6K1 and 4E-BP1 mRNA expressions in the medium with Leu concentration of 2 mM were significantly higher than that in 0.2 mM group (p < 0.05). There was no difference between the medium with Gly-Leu concentration of 2 mM and 0.2 mM on the TOR, S6K1 and 4E-BP1 mRNA expressions (p > 0.05). In conclusion, Leu significantly increases TOR, S6K1 and 4E-BP1 mRNA expressions of skeletal muscle satellite cells, but Gly-Leu peptide has no effect on them.

1. The present study was conducted to investigate whether brain somatostatin increases feed intake in neonatal chickens. The mediating role of neuropeptide Y receptors on feed intake induced by somatostatin was investigated. 2. In this study, seven experiments were designed, each with four treatment groups (n = 44 in each experiment). In Experiment 1, chicks received control solution and 0.5, 1 and 2 nmol of somatostatin through intracerebroventricular (ICV) injection. In experiments 2, 3 and 4, chickens were ICV injected with control solution and 1.25, 2.5 and 5 μg of B5063 (NPY1 receptor antagonist), SF22 (NPY2 receptor antagonist) and SML0891 (NPY5 receptor antagonist), respectively. In experiment 5, 6 and 7 chickens received ICV injection of B5063, SF22, SML0891, with a co-injection of + somatostatin, control solution and somatostatin. The cumulative feed intake was measured until 120 min post injection. 3. Somatostatin significantly increased feed intake in FD3 chicks. Both B5063 and SML0891 dose-dependently decreased feed intake compared with the control group, while SF22 led to a dose-dependent increase in feed intake. In addition, the hyperphagic effect of somatostatin significantly decreased with co-injection of B560 plus somatostatin (p < 0.05), but SF22 and SML0891 had no effect on feed intake induced by somatostatin in chicks (p > 0.05). 4. Based on the results of this study, it is likely that somatostatin increased feed intake and NPY1 receptor acts as a mediator in hyperphagic effect of somatostatin in neonatal chicks.

The present study was designed to determine the effect of central injection of Nesfatin-1 and corticotropin and histaminergic systems on food intake in neonatal meat-type chicks. In this study, 7 experiments were designed, each with 4 treatment groups. In experiment 1, four groups of chicks received the ICV injection of (A) phosphate-buffered saline (PBS), (B) Nesfatin-1 (10 ng), (C) Nesfatin-1 (20 ng) and (D) Nesfatin-1 (40 ng). In experiment 2, (A) PBS, (B) Astressin-B (CRF1/CRF2 receptors antagonist; 30 µg), (C) Nesfatin-1 (40 ng) and (D) Nesfatin-1 + Astressin-B were injected. In experiments 3-6, chicken received ICV injection of the Astressin2-B (CRF2 receptor antagonist; 30 µg), α-FMH (alpha fluoromethyl histidine; as inhibitor of histidine decarboxylase, 250 nmol), Chlorpheniramine (histamine H1 receptors antagonist, 300 nmol), Famotidine (histamine H2 receptors antagonist, 82 nmol) and Thioperamide (histamine H3 receptors antagonist, 300 nmol) instead of the Astressin-B. Then the cumulative food intake measured until 120 min post-injection. According to the results, ICV injection of Nesfatin-1 dose dependently decreased food intake in neonatal chicks (P < 0.05). Co-injection of the Nesfatin-1 and Astressin-B (CRF1/CRF2) inhibited Nesfatin-1 induced hypophagia (P < 0.05). ICV inejction of the Nesfatin-1 + Astressin-B significantly inhibited the effect of Nesfatin-1 on food intake (P < 0.05). In addition, α-FMH and chlorpheniramine attenuated Nesfatin-1-induced hypophagia in chicks (P < 0.05); while thioperamide significantly amplified the effect of Nesfatin-1 on food intake in chicks (P < 0.05). These results suggested Nesfatin-1 has an anorectic effect in 3-hour food deprived neonatal meat-type chicks and this effect was mediated by corticotropin CRF1/CRF2 as well as histamine H1 and H3 receptors.