Hongchao Jiao

Thermoregulation responses of broiler chickens to humidity at different ambient temperatures. I. One week of age

Three trials were conducted to investigate the effect of RH (35, 60, and 85%) on thermoregulation of 1-wk-old broiler chickens at different temperatures (35, 30, and 25 degrees C). The response to humidity in rectal temperature and plumage temperature at the back and breast within 24 h after exposure were recorded at 5 time points (1,4,8,16, and 24 h). Humidity affected the thermoregulation of 1-wk-old broiler chickens by redistributing heat within the body at high, low, and thermoneutral temperatures. The redistribution of heat resulted in decreased rectal temperature and increased peripheral temperature, which were, respectively, beneficial and unfavorable at high and low temperatures. These results suggested that feedback effects of surface temperature on core temperature also exist in poultry, as already observed in mammals, and could be induced not only by changed ambient temperature but also by the changes in humidity at high temperature. The disturbance of thermal equilibrium could not be established solely by changes in RT, but rather core and surface temperatures had to be considered. The daily rhythms in rectal and surface temperatures were affected by humidity.

Corticosterone administration and high-energy feed results in enhanced fat accumulation and insulin resistance in broiler chickens

1. Two experiments were conducted to investigate the effects of exogenous corticosterone administration (30 mg/kg diet) and dietary energy level on feed or energy intake and fat deposition in broiler chickens of 1 and 4 weeks of age. 2. Corticosterone treatment significantly suppressed body weight (BW) gain and reduced feed and caloric efficiencies. The retarded growth may conceal the stimulatory effect of corticosterone on feed consumption or metabolisable energy (ME) intake. A high-energy diet may increase energy intake and partially alleviate the suppressing effect of corticosterone on growth of broilers. 3. Corticosterone administration promoted the conservation of energy stores as fat at both abdominal and subcutaneous sites and this process occurred regardless of dietary energy level in ad libitum feeding status. A high-energy diet increased fat accumulation and showed no significant interaction with corticosterone treatment. 4. The suppressed development of breast and thigh muscles by corticosterone treatment was observed only in 1-week-old chickens fed on the low-energy diet. In contrast, the yield of breast muscle but not thigh muscle was significantly decreased by corticosterone in 4-week-old chickens, suggesting that the tissue specificity to corticosterone challenge is age dependent. 5. Plasma concentrations of glucose, insulin, triglyceride, non-esterified fatty acids (NEFA) and very low density lipoprotein were increased by corticosterone treatment regardless of diet treatment. A high-energy diet increased plasma levels of NEFA and resulted in hyperinsulinism in 4-week-old chickens but not in 1-week-old chickens. 6. Lipoprotein lipase (LPL) activities in adipose tissues may have been up-regulated by corticosterone treatment and showed tissue specificity. The increased LPL activities at ad libitum feeding status were not necessarily linked with the increased fat accumulation in corticosterone challenged chickens. 7. Corticosterone resulted in augmented energy consumption and altered energy redistribution toward lipid deposition. The induced insulin resistance and enhanced hepatic de novo lipogenesis by corticosterone are likely to be responsible for the increased fat deposition.

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.

Increased de novo lipogenesis in liver contributes to the augmented fat deposition in dexamethasone exposed broiler chickens (Gallus gallus domesticus)

Effect of dexamethasone (DEX, a synthetic glucocorticoid) on lipid metabolism in broiler chickens (Gallus gallus domesticus) was investigated. Male Arbor Acres chickens (1 wk old, n=30) were injected with DEX or saline for 1 wk, and a pair-fed group was included. DEX administration resulted in enhanced lipid deposition in adipose tissues. Plasma insulin increased about 3.3 fold in DEX injected chickens as against the control and hepatic triglyceride was higher as compared with the pair-fed chickens. In DEX injected chickens, the hepatic activities of malic enzyme (ME) and fatty acid synthetase (FAS) were significantly increased, while the mRNA levels of acetyl CoA carboxylase (ACC), ME, and FAS were significantly up-regulated, compared with the control. Although the mRNA levels of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor-gamma (PPARgamma) and adipose triglyceride lipase (ATGL) genes in adipose tissue were not affected by DEX injection, ME activity and mRNA levels in abdominal fat pad of chickens treated with DEX are higher than those of control chickens. The results indicated that the increased hepatic de novo lipogenesis and in turn, the increased circulating lipid flux contributes to the augmented fat deposition in adipose tissues and liver in DEX-challenged chickens. The results suggest that glucocorticoids together with the induced hyperinsulinemia should be responsible for the up-regulated hepatic lipogenesis.

Heat stress impairs mitochondria functions and induces oxidative injury in broiler chickens.

The objective of this study was to explore the linkage of oxidative stress occurring in mitochondria, skeletal muscles, and plasma in heat stress-challenged broilers. At d 35, 24 broilers were randomly assigned to 2 treatments: rearing at high temperature (32 ± 1°C; heat stress group) or normal temperature (21 ± 1.2°C; control) for 7 d. The oxidative damage of lipid, DNA, and protein and the activities of antioxidative enzymes were measured, respectively, in plasma, skeletal muscles (breast and thigh muscles), and skeletal muscle mitochondria. The result showed that heat exposure increased (P < 0.01) plasma concentrations of thiobarbituric acid reacting substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) whereas it deceased total antioxidant capacity (P < 0.05) and ability to inhibit hydroxyl radicals (AIHR; P< 0.001). Protein carbonyl and TBARS levels were increased (P < 0.001) by heat stress in breast and thigh muscles. In skeletal muscle mitochondria, heat stress increased (P < 0.05) 8-OHdG and suppressed AIHR. Plasma activity of superoxide dismutase (SOD) was increased (P< 0.001) whereas glutathione peroxidase (GSH-Px) was suppressed by heat stress (P < 0.001). Heat exposure increased SOD and catalase activities in breast muscle (P < 0.01) but the reverse was true in thigh muscle (P < 0.05). Glutathione peroxidase was increased in thigh muscle (P < 0.001) but was not changed in breast muscle (P > 0.05). Heat stress increased SOD (P < 0.05) and decreased GSH-Px activities (P < 0.05) of mitochondria regardless of muscle types. Plasma allantoin level increased (P < 0.01) correspondingly with urate (P < 0.001) in heat-stressed broilers, indicating that urate could serve as an antioxidant to enhance the antioxidative capacity during stress in a concentration-dependent manner. The activities of respiratory chain complexes I and III were estimated in skeletal muscle mitochondria. Mitochondrial complex I activity was suppressed (P < 0.01) by heat exposure in breast and thigh muscles but complex III activity was elevated only in breast muscle (P < 0.01) of heat-stressed broiler. The fatty acid composition in skeletal muscle was not influenced by heat stress. In conclusion, suppressed mitochondrial complex I activity is associated with oxidative stress induced by heat exposure, which, in turn, is linked with the oxidative damages in muscle tissues and plasma.

Effect of Heat Exposure on Gene Expression of Feed Intake Regulatory Peptides in Laying Hens

The aim of this paper was to investigate the effect of heat stress on the regulation of appetite-associated genes in laying hens. Forty eight laying hens were randomly divided into two circumstances: high (31 ± 1.5°C; relative humidity, 82.0 ± 2.2%) or normal (20 ± 2°C, control; relative humidity, 60.1 ± 4.5%) ambient environment. Heat stress decreased body weight gain (P < 0.01), feed intake (P < 0.01), laying rate (P < 0.05), average egg mass (P < 0.01), egg production (P < 0.01), shell thickness (P < 0.01), and feed efficiency (P < 0.05). High ambient temperature decreased plasma uric acid (P < 0.05). Heat stress significantly increased mRNA levels of ghrelin and cocaine- and amphetamine-regulated transcript (P < 0.05) and decreased mRNA levels of cholecystokinin (P < 0.05) in the hypothalamus. Heat stress significantly increased (P < 0.05) mRNA levels of ghrelin in the glandular stomach and jejunum but significantly decreased (P < 0.05) mRNA levels of cholecystokinin in the duodenum and jejunum. In conclusion, heat stress plays a unique role in some special neuropeptides (e.g., ghrelin, cocaine- and amphetamine-regulated transcript, and cholecystokinin), which might participate in the regulation of feed intake in laying hens under high ambient temperature.

Stocking density affects the growth performance of broilers in a sex-dependent fashion.

The effects of stocking density, sex, and dietary ME concentration on live performance, footpad burns, and leg weakness of broilers were investigated. A total of 876 male and 1,020 female 1-d-old chicks were placed in 24 pens to simulate final stocking density treatments of 26 kg (LSD; 10 males or 12 females/m(2)) and 42 kg (HSD; 16 males or 18 females/m(2)) of BW/m(2) floor space. Two series of experimental diets with a 150 kcal/kg difference in ME concentration (2,800, 2,900, and 3,000 or 2,950, 3,050, and 3,150 kcal of ME/kg) were compared in a 3-phase feeding program. The HSD treatment significantly decreased BW gain and feed conversion ratio (FCR). The HSD chickens consumed less feed by 35 d of age; thereafter, the reverse was true. Male chickens had significantly higher feed intake (FI), BW gain, and FCR compared with females. A significant interaction was found of stocking density and age for FI, BW gain, and FCR. Compared with LSD treatment, HSD broilers had a higher FI and a lower FCR from 36 to 42 d of age. Stocking density, sex, and age had a significant interaction for BW gain and FCR. Female broilers had worse BW gain and FCR when stocked at high density from 36 to 42 d of age. Stocking density had no significant influence on breast, thigh, or abdominal fat yield. Female broilers had significantly higher breast yield and abdominal fat. Male broilers and HSD treatment had high footpad burn and gait scores. A low ME diet increased footpad burn score but had no effect on gait score. The result indicated that stocking density had a more severe effect on the growth of male broilers before 35 d of age. Female broilers need more space than males at similar BW per square meter near marketing age. The incidence and severity of leg weakness are associated with sex, diet, and stocking density. This result suggests that the deteriorated effect of high stocking density is sex and age dependent.

Dexamethasone-induced hepatic lipogenesis is insulin dependent in chickens (Gallus gallus domesticus).

Hepatic lipogenesis-induced de novo by glucocorticoids (GCs) is associated with the development of obesity and diabetes mellitus. The interaction of GCs and insulin in the regulation of hepatic lipogenesis remains unclear. The effect of exogenous GC administration on hepatic lipogenesis and fat deposition was studied in broiler chickens (Gallus gallus domesticus), and the role of insulin in the effect of GCs on hepatic lipogenesis was evaluated. Dexamethasone (DEX, 2 mg/kg body mass (BM)) administration for 3-d resulted in BM loss and increased liver and cervical adipose tissue mass compared to control and pair-fed counterparts. DEX treatment significantly (P < 0.05) increased plasma level of insulin in either the fed or fasting state, whereas plasma glucose level was only increased in the fed state. In fasted chickens, DEX treatment significantly (P < 0.01) upregulated the hepatic mRNA levels of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). In the fed state, the mRNA levels of ACC and FAS were not significantly influenced by DEX treatment, nor was FAS activity. In cultured primary hepatocytes, combined DEX and insulin significantly upregulated the transcription of the genes for FAS (1.34-fold) and malic enzyme (1.72-fold). By contrast, the expression of sterol response element-binding protein-1 (SREBP-1) was significantly upregulated by insulin (1.67-fold) regardless of DEX. In abdominal adipose tissue, DEX treatment had no significant (P>0.05) effect on the activities and transcription of FAS. The expressions of lipoprotein lipase and peroxisome proliferator-activated receptor-γ were not significantly (P>0.05) affected by DEX treatment in either the fasting or fed state. The results indicate that DEX increased hepatic de novo lipogenesis via the increased activity and expression of lipogenic enzymes. Insulin-activated gene expression for SREBP-1 is suggested to be involved in stress-augmented hepatic lipogenesis.

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.

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.