Lipopolysaccharide inhibits hypothalamic Agouti-related protein gene expression via activating mechanistic target of rapamycin signaling in chicks.

Lipopolysaccharide (LPS) induces profound anorexia in birds. However, the neuronal regulatory network underlying LPS-provoked anorexia is unclear. To determine whether any cross talk occurs among hypothalamic mechanistic target of rapamycin (mTOR) and LPS in the regulation of appetite, we performed an intracerebroventricular injection of rapamycin (an mTOR inhibitor) on LPS-treated chicks. The results indicate that peripheral administrations of LPS decreased the agouti-related protein (AgRP) mRNA level, but increased the phosphorylated mTOR and nuclear factor-кB (NF-кB) protein level. Blocking mTOR significantly attenuated LPS-induced anorexia, AgRP suppression, and p-NF-кB increase. Thus, the results suggest that LPS causes anorexia via the mTOR-AgRP signaling pathway, and mTOR signaling is also associated with the regulation of LPS in p-NF-кB.

Different effects of probiotics and antibiotics on the composition of microbiota, SCFAs concentrations and FFAR2/3 mRNA expression in broiler chickens.

AIMS: The aims of this study were to investigate the effects of probiotics and antibiotics on microbial composition, short chain fatty acids (SCFAs) concentration and free fatty acid receptor 2/3 (FFAR2/3) expression in boiler chickens. METHODS AND RESULTS: A total of 150 1-day-old male broilers were randomly allocated into three groups, control (CON) group, probiotics (PB) group and antibiotics (ATB) group. Results indicated that PB improved the average body weight from 1 to 21 days and feed intake from 21 to 42 days (P < 0·05), while ATB improved the feed efficiency from 1 to 42 days (P < 0·05). Based on 16s rRNA sequencing, PB treatment increased the amount of kingdom bacteria, and the relative abundance of the main bacteria including acetate and butyrate producing bacteria of phylum Firmicutes, family Ruminococcaceae and genus Faecalibacterium. ATB treatment also increased the relative abundance of phylum Firmicutes, family Ruminococcaceae and Lachnospiraceae, however, it introduced some pathogenic bacteria, such as bacteria of family Rikenellaceae and Enterobacteriaceae. Gas chromatography and mass spectrometry (GC-MS) assay revealed that PB increased acetate and butyrate concentrations at both 21 and 42 days, and propionate at 42 days in the colorectum. Moreover qRT-PCR analysis showed PB treatment significantly activated the FFAR2/3 mRNA expressions. On the contrast, ATB treatment lowered the colorectal propionate at 21 days, and decreased acetate, propionate and butyrate concentrations at 42 days, accompanied with decreased FFAR2/3 mRNA expressions. CONCLUSIONS: Compared to the CON birds, an enriched SCFAs producing bacteria with higher SCFAs contents and activated FFAR2/3 expressions are prominent features of PB birds. However, antibiotics treatment plays the reverse effect compared to PB treatment. SIGNIFICANCE AND IMPACT OF THE STUDY: This study brings a significant idea that less SCFAs concentration may be another reason why the antibiotics inhibit the immune system development and immunity of the body.

Fibroblast growth factor 23 mRNA expression profile in chickens and its response to dietary phosphorus.

In mammals, fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis in kidney by binding α-Klotho, a coreceptor of FGF23. FGF23 mRNA is highly expressed in bone and slightly expressed in liver, and is regulated by dietary phosphorus. Little is known about distribution and regulation of FGF23 mRNA in avian lineage. The expression of FGF23 and its coreceptor α-Klotho in chicken and embryo were investigated by real-time quantitative PCR. The effect of dietary phosphorus on FGF23 expression was measured. 36 laying hens at 25 wk were randomly assigned to three dietary available phosphorus (AP) treatments for 11 days: 0.15% AP (LP), 0.40% AP (MP), and 0.80% AP (HP). We first cloned the full coding sequence of FGF23 by the reverse transcription PCR from chicken liver and calvaria. Bioinformatics analysis indicated that the deduced amino acid sequence was 57-87% identical to FGF23 of other species. In adult chicken FGF23 mRNA was expressed at unexpected higher level in liver than other tissues evaluated, including calvaria, femur, tibia, medullary bone, brain, spleen, duodenum, jejunum, ileum, heart and kidney (P < 0.0001), and α-Klotho was expressed at highest level in kidney. However, in 18-d chicken embryos, FGF23 mRNA level was much higher in tibia than in liver, heart and jejunum (P < 0.0001). Chickens at 2, 25, 50 and 80 wk had higher FGF23 expression in liver than 18-d chicken embryos, whereas chickens at 25 wk had lower FGF23 expression in tibia than 18-d chicken embryos and 2-wk-old chickens. HP diets significantly increased serum inorganic phosphorus level (P < 0.001) and FGF23 expression (P < 0.05) in bone tissue compared with LP diets, however, FGF23 mRNA abundance in liver was not changed significantly (P > 0.05) by dietary phosphorus treatments. In conclusion, FGF23 mRNA expression pattern in chicken was clearly different from that in mammals and dietary phosphorus regulated the expression of FGF23 in a tissue-specific way.

Leucine alters immunoglobulin a secretion and inflammatory cytokine expression induced by lipopolysaccharide via the nuclear factor-κB pathway in intestine of chicken embryos.

The mammalian target of rapamycin (mTOR) has been shown to be involved in lipopolysaccharide (LPS)-induced immune responses in many mammal cells. Here, we suggest that the mTOR pathway is involved in the intestinal inflammatory responses evoked by LPS treatment in chicken embryos. The intestinal tissue from Specific pathogen free chick embryos was cultured in the presence of LPS for 2 h. Secretory immunoglobulin A (sIgA) concentrations, messenger RNA (mRNA) expression of cytokines, and protein levels of nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), mTOR and p70 ribosomal S6 kinase (p70S6K) were determined. The results showed that LPS treatment increased sIgA concentrations in a dose-dependent manner. The mRNA levels of interleukine (IL)-6, IL-8, IL-10, tumor necrosis factor-α and Toll-like receptor (TLR) 4 were upregulated by LPS treatment (P<0.05). Lipopolysaccharide increased the phosphorylation of Jun N-terminal kinase (JNK), p38 MAPK and NF-κB (P<0.05) while decreasing the phosphorylation level of mTOR (P<0.05). Supplementation of leucine at doses of 10, 20 and 40 mM dose-dependently decreased sIgA production. Leucine supplementation at 40 mM restored the phosphorylation level of mTOR and p70S6K while suppressing the phosphorylation levels of NF-κB (P<0.05) and partially down-regulating the phosphorylation of p38 MAPK and JNK. The transcription of IL-6 was significantly decreased by leucine supplementation. These results suggested that leucine could alleviate LPS-induced inflammatory responses by down-regulating NF-κB signaling pathway and evoking mTOR/p70S6K signaling pathway, which may involve in the regulation of the intestinal immune system in chicken embryos.

Live performance, carcass characteristic and blood metabolite responses of broilers to two distinct corn types with different extent of grinding.

The major objective of this research was to establish the main and interactive effects of corn type and extent of grinding on broiler performance including carcass characteristics. A completely randomized experimental design with a 2 (corn type) × 2 (fine and coarse) factorial arrangement, each with six replicates of 45 male Ross chicks, was applied. Experimental diets, containing dent or hard corn, were formulated with two extents of grinding (3.00 or 6.00 mm screens) for three growing phases. In comparison with dent corn, the hard corn increased body weight (BW) gain and thigh muscle yield (p < 0.05), while decreasing feed conversion ratio (p < 0.01) and abdominal fat deposition (p < 0.05), some aspects of which were age-dependent and appeared to vary with extent of grinding. Coarser grinding increased the weight of proventriculus (p < 0.01), gizzard (p < 0.05) and small + large intestine (p < 0.10) relative to BW, particularly towards market size. These results suggest that feeding hard corn or large-particle-size corn have some favourable effects on growth performance or gastrointestinal development for finishing broilers.

Ovalbumin expression in the oviduct magnum of hens is related to the rate of egg laying and shows distinct stress-type-specific responses.

Three trials were performed to evaluate the association of ovalbumin (OVA) abundance in the oviduct magnum with egg production and the underlying regulatory mechanism by glucocorticoids. In trial 1, twenty Hy-Line Brown layers (56-60 weeks of age) with different combinations (n = 5/combination) of laying rate (high or low) and egg weight (high or low) were selected from an initial group of 300. An upregulated expression of magnum OVA was observed (p < 0.05) in hens with higher laying rate, regardless of egg weight. In trial 2, eighty Hy-Line Brown layers (80-90 weeks of age) were subjected to the forced moulting (n = 8). The abundance of OVA transcript and protein in the magnum was significantly decreased during moulting (p < 0.01), and the same was true for laying rate (p < 0.01) and serum oestrogen (p < 0.05). In trial 3, forty-five 56-week-old Hy-Line Brown layers were kept individually (n = 15) in the following conditions for 10 days: constant optimal ambient temperature at 23 °C and ad libitum feeding, high ambient temperature at 32 °C for 6 h/day (10:00-16:00) and ad libitum feeding (32AL), and constant optimal ambient temperature at 23 °C and pair-fed to the 32AL hens. In spite of elevated corticosterone in circulation, OVA synthesis, blood oestrogen and laying rate were not affected by heat exposure (p > 0.05). These results allow concluding that OVA expression in the oviduct magnum of hens is related to the rate of egg laying and shows distinct stress-type-specific responses.

Rapamycin, a specific inhibitor of the target of rapamycin complex 1, disrupts intestinal barrier integrity in broiler chicks.

To uncover the molecular mechanisms underlying the intestinal barrier integrity, this study determined whether the rapamycin (RAPA)-sensitive target of rapamycin complex 1 (TORC1) pathway was involved in this process. Three groups of 4-day-old male chicks were randomly subjected to one of the following treatments for 6 days: high-dose RAPA [a specific inhibitor of TORC1; an intraperitoneal injection of 1.0 mg/kg body weight (BW), once daily at 09:00 hours], low-dose RAPA (0.4 mg/kg BW) and RAPA vehicle (control). Results showed that the RAPA treatment increased mortality, while decreasing villus height (p < 0.01), claudin 1 expression, content of immunoglobulin A (IgA), extent of TORC1 phosphorylation (p < 0.05), ratio of villus height to crypt depth (p < 0.01), and population of IgA-positive B cells in intestinal mucosa, particularly for the jejunum. Some aspects of these responses were dose dependent and appeared to result from weight loss. Together, RAPA exerts the expected inhibition of small intestinal development and IgA production in birds, suggesting the important role of TORC1 in gut barrier integrity.

Dietary supplementation with sodium bicarbonate improves calcium absorption and eggshell quality of laying hens during peak production.

The advantage of supplemental sodium bicarbonate (NaHCO3) on eggshell quality in laying hens changes with age. Besides increasing calcium (Ca) secretion in the eggshell gland, it may improve Ca absorption in the intestine or kidney. Hy-Line Brown layers (n = 384), 25 weeks of age, were allocated to two treatment groups in two experiments, each of which included 4 replicates of 24 hens. Hens were fed a basal diet (control) or the basal diet containing 3 g NaHCO3 g/kg for 50 or 20 weeks in Experiment 1 or 2, respectively. A 24-h continuous lighting regimen was used to allow hens to consume the dietary supplements during the period of active eggshell formation. In Experiment 1, particularly from 25 to 50 weeks of age, and in Experiment 2, NaHCO3 supplementation favoured hen-d egg production at the expense of lower egg weight. The increased eggshell thickness should have nothing to do with the additional eggshell formation, because of the unchanged egg mass and daily eggshell calcification. At 35 weeks of age in both experiments, NaHCO3 supplementation increased duodenal expression of calbindin-d28k (CaBP-D28k) protein, contributing to higher Ca retention and balance. From 50 to 75 weeks of age in Experiment 1, the hens had little response to NaHCO3 supplementation and showed a negative trend on eggshell thickness and strength. It is concluded that dietary supplementation with 3 g NaHCO3 g/kg improves Ca absorption and eggshell quality of laying hens during the peak but not late production period, with the introduction of continuous lighting.

Increased hepatic yolk precursor synthesis, secretion and facilitated uptake by follicles are involved in the rejuvenation of reproductive performance of molted hens (Gallus gallus domesticus).

Molt, a natural behavior that is initiated at the end of a lay cycle in birds, is implicated in the regression of the reproductive system in birds followed by a rejuvenation of egg-laying potential. The aim of the present study was to evaluate the physiological basis for the apparent rejuvenation of egg production that occurs following molting. Eighty-three-week-old Hy-line hens, were obtained and subjected to forced molting. Blood and tissue samples were obtained at the beginning of molt (at 83 weeks of age), during molt (at 85 weeks of age) and postmolt (at 89 weeks of age). The laying performance, egg quality, blood parameters and gene expression in the liver and the ovary were investigated before, during and after molt. There was an obvious increase in the postmolt laying rate from 70% premolt to 93% postmolt. Eggshell thickness, albumin height, Haugh unit and egg shape index were all significantly improved after molt. The circulating levels of estrogen and progesterone were lower in the postmolt hens, whereas the concentrations of luteinizing hormone and follicle stimulating hormone were not significantly affected by molt. These results indicate that enhanced hepatic yolk precursor synthesis and secretion contribute to increased postmolt laying performance. Molt enhanced the sensitivity of sex hormones in F1 follicles. Augmented gene expression in the ovary was involved in the rejuvenation of the reproductive performance of molted hens. These results suggest that facilitated yolk-precursor uptake by follicles is involved in the rejuvenation of the reproductive performance of molted hens.

Cool perches improve the growth performance and welfare status of broiler chickens reared at different stocking densities and high temperatures.

The present study investigated the interaction of stocking density and cool perch availability on broiler chickens raised at high ambient temperature (>30.8°C). Behavior, live performance, and the incidence of footpad and hock burns and abdominal plumage damage were investigated over a 4-wk experimental period. A total of 1,152 one-day-old Arbor Acres chicks were subjected to a 2 (cool perches) × 3 (stocking densities) factorial arrangement of treatments. From 1 d of age, birds were provided with or without cool perches at each of 3 stocking densities (12, 16, or 20 birds/m(2); low, medium, or high stocking density, respectively) and corresponded to 48, 64, and 80 birds per pen. The perch design provided 380 cm of linear perching space in each treatment pen. The results showed that high stocking density decreased the growth (P < 0.05) and welfare (P < 0.01) of broilers. Cool perch availability increased BW gain and feed conversion efficiency of broilers (P < 0.05) regardless of stocking density. The birds' use of cool perches increased with age (P < 0.01) and decreased with higher stocking density (P < 0.05). The accessibility of cool perches changed birds' behavior patterns (P < 0.01) and reduced footpad or hock burns and damage to abdominal plumage (P < 0.05). These results suggest that cool perches have a favorable effect on the performance and welfare of broilers.

Skeletal muscle fatty acids shift from oxidation to storage upon dexamethasone treatment in chickens.

The effect of an exogenous glucocorticoid on the lipid metabolism and fatty acid pattern of skeletal muscle in broiler chickens (Gallus gallus domesticus) was investigated in vivo and in vitro. Male Arbor Acres chickens were subjected to dexamethasone (DEX) treatment for 3days. We found that DEX retarded body growth, facilitated lipid accumulation in adipose and skeletal muscle tissues, and elevated the thigh monounsaturated fatty acids (MUFA) to saturated fatty acids (SFA) ratio at fasted state. DEX-treated chickens exhibited increased stearoyl-CoA desaturase-1 (SCD1) activity and decreased carnitine palmitoyltransferase-1 (CPT1) activity in the thigh muscle under fasting conditions and in primary cultured myoblasts. Phosphorylation of AMP-activated protein kinase alpha at Thr172 did not occur in vivo but was increased in vitro by DEX. In cells exposed to DEX, fatty acid transport protein-1 mRNA expression and fatty acid storage were enhanced while fatty acid oxidation was repressed. In conclusion, in oxidative muscle of fasted chickens, DEX stimulated uptake of myocellular fatty acids which was stored with the modified MUFA to SFA ratio in a process that maybe involved SCD1 activation. The altered fatty acid composition together with the inactivation of CPT1 showed an increased tendency towards fatty acid accumulation as opposed to oxidation. These findings provide important insight concerning the influence of glucocorticoids on lipid metabolism.

Altered gene and protein expression of glucose transporter1 underlies dexamethasone inhibition of insulin-stimulated glucose uptake in chicken muscles.

A study was performed to characterize the effects of dexamethasone (DEX) and insulin administration on gene expression of glucose transporters (GLUT) in chicken (Gallus gallus domesticus) skeletal muscles and in cultured embryonic myoblasts. Three groups of 1-wk-old male chickens were randomly subjected to one of the following treatments for 7 d: DEX (a subcutaneous injection of 1 mg/kg BW, twice daily at 0800 h and 2000 h), controls (injected with saline), and pair-fed controls (restricted to the same feed intake as for the DEX treatment). Expressions of GLUT-1, GLUT-3, GLUT-8, and 18S rRNA mRNA were determined by quantitative reverse transcription PCR in the pectoralis major (PM) and biceps femoris (BF) muscles. Using chicken embryonic myoblasts (CEM), the interaction between DEX (200 nM) and insulin (100 nM) administration was evaluated on GLUT gene and GLUT-1 protein expressions and 2-deoxy-D-[1, 2-(3)H]-glucose (2-DG) uptake. Myoblasts were incubated with serum-free medium for 3 h in the presence or absence of insulin (0, 0.02, 0.1, 0.5, and 2.5 µM). Although GLUT-1 is not considered an insulin-responsive GLUT in mammals, this study shows that insulin stimulated 2-DG uptake and GLUT-1 mRNA and protein expression in CEM (P < 0.0001), suggesting that both are regulated in chicken skeletal muscle. Dexamethasone inhibited insulin-stimulated glucose uptake in CEM (P < 0.0001), likely accounting for insulin resistance in skeletal muscles. The results of the present study indicate that the altered GLUT-1 gene and protein expression may contribute to the insulin resistance induced by DEX treatment in chicken muscles.

Cool perch availability improves the performance and welfare status of broiler chickens in hot weather.

A study was conducted to determine whether water-cooled perches would be preferred by commercial broilers exposed to a hot ambient environment, and subsequently, whether utilization of these perches would improve performance and the well-being of birds, beyond those provided by normal perches. Four hundred and thirty-two 14-d-old male chickens from a commercial fast-growing strain (Arbor Acres) were housed in the following conditions: 1) cool perches, 2) normal perches, and 3) control pens with no perches. The results showed that there was greater use of cool perches than normal perches for broiler chickens during summer (F1, 4=125, P=0.0004). Cool perches increased BW gain (F2, 6=5.44, P=0.0449) and breast (F2, 24=3.31, P=0.0539) and thigh muscle yields (F2, 24=6.29, P=0.0063), while decreasing abdominal fat deposition (F2, 24=7.57, P=0.0028), cooking loss (pectoralis major, F2, 24=3.30, P=0.0542; biceps femoris, F2, 24=3.42, P=0.0493), percentage of panting birds (F2, 6=102, P<0.0001), and scores of footpad (F2, 6=122, P<0.0001) and hock (F2, 6=68.2, P<0.0001) burn, and abdominal plumage condition (F2, 6=52.0, P=0.0002), particularly toward the end of the rearing period. In contrast, normal perches hardly affected growth performance, carcass composition, meat quality and behavioral patterns, and appeared to worsen the welfare status, including footpad and hock burns and abdominal plumage condition, due to a lower occupancy rate. Cool perches offer a thermoregulatory and performance advantage to broilers exposed to a hot environment and appear to be a management strategy for improving the production and well-being of commercial broilers.

Dexamethasone facilitates lipid accumulation in chicken skeletal muscle.

The effects of glucocorticoid on lipid metabolism of broiler chicken (Gallus gallus domesticus) skeletal muscle were investigated. Male Arbor Acres chickens (35 days old) were subjected to dexamethasone treatment for 3 days. We found that dexamethasone retards body growth while facilitating lipid accumulation. In M. pectoralis major (PM), dexamethasone increased the expression of glucocorticoid receptor (GR), fatty acid transport protein 1 (FATP1), heart fatty acid-binding protein (H-FABP) and long-chain acyl-CoA dehydrogenase (LCAD) mRNA and decreased the expression of liver carnitine palmitoyltransferase 1 (L-CPT1), adenosine-monophosphate-activated protein kinase (AMPK) α2 and lipoprotein lipase (LPL) mRNA. LPL activity was also decreased. In M. biceps femoris (BF), the levels of GR, FATP1 and L-CPT1 mRNA were increased. AMPKα (Thr172) phosphorylation and CTP1 activity of skeletal muscle were decreased by dexamethasone. In fed chickens, dexamethasone enhanced very low-density lipoprotein receptor (VLDLR) expression and AMPK activity in muscle, but it impaired the expression of LPL and L-CPT1 mRNA and LPL activity in PM and augmented the expression of GR, LPL, H-FABP, L-CPT1, LCAD and AMPKα2 mRNA in BF. Adipose triglyceride lipase (ATGL) protein expression was not affected by dexamethasone. In conclusion, in the fasting state, dexamethasone-induced-retarded fatty acid utilisation may be involved in the augmented intramyocellular lipid accumulation in both glycolytic (PM) and oxidative (BF) muscle tissues. In the fed state, dexamethasone promoted the transcriptional activity of genes related to lipid uptake and oxidation in muscles. Unmatched lipid uptake and utilisation are suggested to be involved in the augmented intramyocellular lipid accumulation.

Dexamethasone alters the expression of genes related to the growth of skeletal muscle in chickens (Gallus gallus domesticus).

Glucocorticoids (GCs) are involved in the muscle wasting caused by trauma, inactivity, and stress. In the present study, three experiments were conducted to investigate the effect of GCs on the expression of genes related to muscle development in chickens. Broilers at 7 or 35 days of age were subjected to dexamethasone (DEX) treatment (2 mg/kg body mass (BM)) for 3 or 7 days. The expression levels of genes such as IGF1, IGF1 receptor, MSTN, WW domain containing E3 ubiquitin (UB) protein ligase 1, myogenic determining factor, and myogenic factor 5 were measured. The results showed that BM gain was significantly suppressed by DEX treatment. The plasma level of insulin was increased (P<0.05) by DEX treatment at feeding, whereas IGF1 was decreased (P<0.05). The expression of genes in the IGF1, myostatin, and UB-proteasome (UBP) pathways were altered by DEX treatment in age- and exposure time-related ways. These results suggest that GCs suppress IGF1 and upregulate myostatin and/or activated myostatin and the UBP pathway, which might be the source of the effect of GCs on muscle development.

Vitamin E supplementation alleviates the oxidative stress induced by dexamethasone treatment and improves meat quality in broiler chickens.

In the present study, the effects of long-term exogenous glucocorticoids administration and dietary supplementation of alpha-tocopheryl acetate on the induction of lipid peroxidation in skeletal muscle were investigated. Male broiler chicks were randomly assigned to 2 diet treatments: the basal diet supplemented with 20 (low level of vitamin E) or 200 (high level of vitamin E) mg of vitamin E (as DL-alpha-tocopheryl acetate)/kg of diet. At 35 d of age, the chickens in each dietary treatment were randomly divided into 3 groups of 30 chickens and subjected to the following treatments: daily s.c. injection of dexamethasone (DEX, 2 mg/kg of BW) for 6 d, sham injection of saline (control), or the sham-treated pair-fed control that maintained the same feed intake as DEX treatment (pair-control). The results showed that the growth of chickens was suppressed by DEX, whereas it was improved by the high level of vitamin E treatment. The DEX treatment resulted in augmented plasma concentrations of TBA reacting substances. Muscle TBA reacting substances levels were higher in DEX chickens at both 24- and 48-h time points postslaughter. Vitamin E supplementation suppressed the formation of lipid peroxidation in both plasma and skeletal muscle tissues. Muscle activity of superoxide dismutase was significantly increased by DEX treatment in both musculus pectoralis major and musculus biceps femoris and maintained as such during the initial 48 h postmortem. The result of the present study indicated that DEX treatment increased the saturation level of skeletal muscle fatty acids. These results suggest that vitamin E supplementation was favorable for the performance of broiler chickens by alleviating the oxidative stress induced by DEX treatment.

Effects of L-arginine supplementation on glucose and nitric oxide (NO) levels and activity of NO synthase in corticosterone-challenged broiler chickens (Gallus gallus).

In the present study, three experiments were conducted to investigate the effect of oral supplementation of l-arginine (ARG) on the disposal of glucose in stressed-broiler chickens (Gallus gallus domesticus). In all the three experiments, the broiler chickens were randomly subjected to one of the four treatments at the beginning of the experiments: oral administration of saline, glucose (2.0g/kg body weight, BW), l-arginine (0.5g/kg BW) or mixed solution (2.0g glucose+0.5g arginine/kg BW). Immediately after the oral treatment, the experimental chickens were subcutaneously injected with corn oil (Experiment 1), corticosterone (CORT, 4mg/kg BW, Experiment 2) or insulin (1U/kg BW, Experiment 3), respectively. Blood samples were obtained at the beginning (0-h), 0.5-, 1- and 2-h time points after injection and the levels of plasma glucose, urate, nitric oxide (NO) and activity of NO synthase (NOS) were measured. The results showed that plasma NO levels and NOS activity were significantly suppressed while glucose and insulin concentrations were increased by CORT treatment. In contrast, insulin administration improved the circulating level of NO and activity of NOS. ARG supplementation could not improve the circulating levels of NO and NOS activity in CORT-challenged chickens and, in turn, the glucose disposal. The result suggests that NO is involved in insulin-mediated glucose transport in chickens, as well as that in mammals. The reduced circulating level of NO resulted from the suppressed activity of NOS rather than the reduced substrate concentration.

Corticosterone administration induces oxidative injury in skeletal muscle of broiler chickens.

The present study had been conducted to explore the effect of corticosterone (CORT) on the induction of lipid peroxidation in skeletal muscle. The experimental chickens were subjected to 1 single s.c. injection of CORT (4 mg/kg of BW). Blood samples were obtained at the beginning and end of a 3-h experimental period. Muscle samples were obtained from musculus pectoralis major and musculus biceps femoris (BF) before and immediately after slaughter, and at 24- and 48-h time points postmortem. The result showed that plasma level of TBA reacting substances (TBARS) was significantly increased, whereas the activity of super-oxide dismutase was decreased after CORT injection. Plasma level of total antioxidant power, as reflected by the ferric reducing-antioxidant power, was increased by CORT administration. The preslaughter level of TBARS could be increased by CORT administration in pectoralis major. In contrast, although the preslaughter level of TBARS was not significantly changed by CORT administration in BF, the augmented TBARS level was detected at 48 h postmortem in BF of CORT chickens. During the period of storage, the concentrations of TBARS increased, whereas ferric reducing-antioxidant power level decreased over time regardless of treatment. In conclusion, the data suggest that elevated CORT due to preslaughter stress would affect the redox balance in skeletal muscle. The result suggested that the oxidative stability during storage of meat is associated with the alteration in muscle physiology induced by CORT administration.

Corticosterone suppresses insulin- and NO-stimulated muscle glucose uptake in broiler chickens (Gallus gallus domesticus).

We evaluated the effects of stress as mimicked by corticosterone (CORT) administration on the uptake of glucose by skeletal muscles (M. fibularis longus) in broiler chickens (Gallus gallus domesticus). The results showed that both chronic (7 d) and short-term (3 h) CORT administration resulted in hyperglycemia and hyperinsulinemia. Plasma level of nitric oxide (NO) and the activity of NO synthase (NOS) were both suppressed by either chronic or acute stress. In vivo CORT treatment could stimulate the in vitro uptake of 2-deoxy-D-[1,2-3H]-glucose (2-DG). Sodium nitroprusside (SNP) administration improved the in vitro uptake of 2-DG in both CORT and control groups. In CORT treatment, however, the stimulating effect of NO on 2-DG uptake was relatively lower compared to control group, whereas it was restored by insulin. Insulin stimulated muscle in vitro 2-DG uptake in either control or CORT group, with the improvement being significantly higher in control chickens. The results indicated that the reduced circulating and muscle level of NO level via the suppression of NOS by corticosterone treatment was involved in the stress-induced insulin resistance. It appears that CORT could suppress the insulin stimulated glucose uptake in skeletal muscle, inducing insulin resistance in broiler chickens. We conclude that NO could stimulate glucose transport in chicken skeletal muscle and that the reduced circulating and muscle level of NO is involved in the insulin resistance induced by corticosterone treatment.

Corticosterone administration and dietary glucose supplementation enhance fat accumulation in broiler chickens.

1. The effects of exogenous corticosterone administration and glucose supplementation on energy intake, lipid metabolism and fat deposition of broiler chickens were investigated. 2. A total of 144 three-d-old male chickens were randomly assigned to one of the following 4 treatments for 7 d: a low energy diet (10.9 MJ ME/kg, 200 g/kg CP) with or without corticosterone (30 mg/kg diet) and drinking water supplemented with glucose (80 g/l) or saccharine (2 g/l, control). 3. Body weight (BW) gain and breast and thigh muscle yields (% body mass) were all significantly decreased by corticosterone treatment. The relative cumulative feed intake (RCFI) and relative ME intake (RMEI), rather than the feed (FI) or ME intake (MEI) were increased by corticosterone administration. Both feed efficiency (FE) and caloric efficiency (CE) were decreased by corticosterone administration. Corticosterone administration had no obvious effect on water consumption. 4. Glucose supplementation had no influence on BW gain and breast and thigh muscle yield (as % of body mass). FI or RCFI was decreased while MEI or RMEI was increased by glucose supplementation. FE was improved by glucose treatment, whereas CE was reduced. 5. Liver weight and abdominal, cervical and thigh fat deposits were all significantly increased by either corticosterone or glucose treatment. 6. Plasma concentrations of glucose, urate, triglyceride, non-esterified fatty acids (NEFA), very low density lipoprotein and insulin were all significantly increased by corticosterone treatment. Glucose supplementation had no obvious influence on any of the measured plasma parameters except for NEFA, which were significantly increased. 7. Lipoprotein lipase activities in either cervical or abdominal adipose tissues, rather than in thigh fat tissue, were significantly elevated by either glucose or corticosterone treatment.