Effects of low-dose oleuropein diet supplementation on the oxidative status of skeletal muscles and plasma hormonal concentration of growing broiler chickens.

1. Oleuropein (Ole) is a major phenolic compound in Olea europaea, with anti-oxidative, anti-obesity, and anti-inflammatory properties. To explore the effect of Ole on the physiology and metabolism of poultry, this study, evaluated the effects of feeding low-dose Ole on the growth performance, metabolic hormonal status, muscle oxidative status in growing broiler chickens.2. Thirty-two 8-day-old chickens were assigned to four different treatments, and fed either 0 (control), 0.1, 0.5, or 2.5 ppm Ole-supplemented diets for 2 weeks.3. There were no differences in the body weight gain, feed consumption, and feed efficiency during the feeding periods between the groups tested. Birds fed Ole 0.5- and 2.5 ppm-supplemented diets exhibited a significant decrease in muscle carbonyl content compared to the control group. In the group fed Ole 0.5 ppm, the mRNA expression levels of mitochondrial ROS-reducing factors: avian uncoupling protein and manganese superoxide dismutase, as well as peroxisome proliferator-activated receptor γ coactivator 1-α, sirtuin-1 and -3 (each of which co-ordinately induce the transcription of the previous two factors) were upregulated compared to the control group, and the changes were independent of plasma noradrenaline and thyroid hormone levels. The group fed Ole-2.5 ppm did not show such transcriptional changes, but exhibited a higher corticosterone concentration.4. This study demonstrates that ingesting a low dose of Ole can reduce muscle oxidative damage, and that the suppression machinery may differ depending on the amount of Ole ingested by growing broiler chickens.

Effects of trehalose supplementation on the growth performance and intestinal innate immunity of juvenile chicks.

Trehalose is composed of two molecules of D-glucose joined by an α,α-1,1 glucosidic linkage and has antioxidative and anti-inflammatory effects. The present study investigated the effect of feeding a trehalose-supplemented diet on the growth performance, as well as the oxidative status and the intestinal innate immunity of juvenile chicks. A total of 16 d-old male broiler chicks were used in this study: two groups of 8 birds were fed on a 0% (control) or 0.5% trehalose-supplemented diet for 18 d. The mean body weight of the trehalose group was significantly greater than that of the control group, but feed efficiency was not altered by feeding the trehalose-supplemented diet. No differences in the levels of lipid peroxidation in skeletal muscle, liver and plasma were observed between the control and trehalose-supplemented groups. The mRNA levels of interferon-γ, tumour necrosis factor-like ligand 1A, interleukin-10, NADPH oxidase 4 and inducible NO synthase were significantly reduced by the trehalose supplementation. Our results suggest that dietary supplementation with trehalose after hatching may have beneficial effects on the growth performance of juvenile chicks, probably by improving their intestinal innate immunity.

Methionine deficiency leads to hepatic fat accretion via impairment of fatty acid import by carnitine palmitoyltransferase I.

1. To clarify the underlying mechanism of hepatic fat accretion due to methionine (Met) deficiency in broiler chickens, the present study investigated the effect of Met deficiency on the hepatic carnitine palmitoyltransferase (CPT) system, which imports fatty acids into mitochondria. 2. Fifteen-d-old male meat-type chickens were fed on either a control diet (containing 0.52 g/100 g Met) or a Met-deficient diet (containing 0.27 g Met/100 g). After a 10-d feeding period, the birds were killed by decapitation and their livers excised to determine hepatic CPT1 and CPT2 mRNA levels and for the related hepatic fatty acid-supported mitochondrial respiration to be measured. 3. Met deficiency decreased body weight gain and feed efficiency and increased hepatic lipid content compared to the control group. Whereas the hepatic CPT2 mRNA level in the Met-deficient group remained unchanged compared to that of the control group, the CPT1 mRNA level was decreased in the Met-deficient group and CPT1-dependent hepatic mitochondrial respiration was impaired. 4. Our results suggest that the hepatic lipid accretion that occurs in response to Met deficiency might be attributable to the impairment of CPT1-mediated fatty acid import into mitochondria.

Electrolysed reduced water decreases reactive oxygen species-induced oxidative damage to skeletal muscle and improves performance in broiler chickens exposed to medium-term chronic heat stress.

1. The present study was designed to achieve a reduction of reactive oxygen species (ROS)-induced oxidative damage to skeletal muscle and to improve the performance of broiler chickens exposed to chronic heat stress. 2. Chickens were given a control diet with normal drinking water, or diets supplemented with cashew nut shell liquid (CNSL) or grape seed extract (GSE), or a control diet with electrolysed reduced water (ERW) for 19 d after hatch. Thereafter, chickens were exposed to a temperature of either 34°C continuously for a period of 5 d, or maintained at 24°C, on the same diets. 3. The control broilers exposed to 34°C showed decreased weight gain and feed consumption and slightly increased ROS production and malondialdehyde (MDA) concentrations in skeletal muscle. The chickens exposed to 34°C and supplemented with ERW showed significantly improved growth performance and lower ROS production and MDA contents in tissues than control broilers exposed to 34°C. Following heat exposure, CNSL chickens performed better with respect to weight gain and feed consumption, but still showed elevated ROS production and skeletal muscle oxidative damage. GSE chickens did not exhibit improved performance or reduced skeletal muscle oxidative damage. 4. In conclusion, this study suggests that ERW could partially inhibit ROS-induced oxidative damage to skeletal muscle and improve growth performance in broiler chickens under medium-term chronic heat treatment.

Time course of ROS production in skeletal muscle mitochondria from chronic heat-exposed broiler chicken.

This study was designed to elucidate physiological changes of skeletal muscle mitochondria from broiler chickens (Gallus gallus) during chronic heat exposure. Chickens (19-day-old) were exposed to either constant heat stress (34 degrees C) or kept at control temperature (24 degrees C) for 14days. Mitochondrial ROS production for control group showed little changes during the experimental periods, whereas that for the heat-stressed group was increased after 3, 5 and 9days of heat exposure and returned to original levels at day 14. Mitochondrial membrane potential in state 4 for heat-stressed birds was higher than those of control birds after 3 and 5days, but was not at day 14. Mitochondrial oxygen consumption rate in state 3 was increased after 3 and 5days, and also returned to original levels by day 14. These results suggest that chronic heat stress induces increased ROS production in skeletal muscle mitochondria, probably via elevation of the membrane potential in state 4, resulting from enhanced oxygen consumption in the initial stage of heat exposure. These physiological changes were no longer observed at day 14, possibly because the animals had acclimatized to environmental heat stress.

Metabolic characteristics and oxidative damage to skeletal muscle in broiler chickens exposed to chronic heat stress.

Emerging evidence has shown that acute heat exposure affects metabolic characteristics and causes oxidative damage to skeletal muscle in birds. Little is known, however, about such phenomena under chronic heat stress conditions. To address this, we designed the present study to determine the influence of cyclic (32 to 24 to 32 degrees C: 32 degrees C for 8 h/d, 32-24-32HS ), and constant (32 and 34 degrees C, 32HS and 34HS, respectively) heat exposure on the metabolic and peroxide status in skeletal muscle of 4-wk-old male broiler chickens. Heat stress, particularly in the 32HS and 34HS groups, depressed feed intake and growth, while cyclic high temperature gave rise to a less severe stress response in performance terms. Malondialdehyde (MDA) levels in skeletal muscle were enhanced (P<0.05) by constant heat treatment; the degree of enhancement was not as large as the changes observed in our previous 'acute' heat stress model. The 3HADH (3-hydroxyacyl CoA dehydrogenase related to fatty acid oxidation) and CS (citrate synthase) enzyme activities were lowered (P<0.05) by both the cyclic and constant 34HS treatments, and constant 34HS group, respectively. These results suggest that chronic heat exposure decreases metabolic oxidation capacity in skeletal muscle of broiler chickens. On exposure to chronic heat stress, GPx activity remained relatively constant, though a temperature-dependent elevation in Cu/Zn-SOD activity was observed, implying that anti-oxidation ability was disturbed by the chronic stress condition. From these results it can be concluded that chronic heat stress did not induce oxidative damage to a major extent. This may probably be due to a decrease in metabolic oxidation capacity or due to a self-propagating scavenging system, though the system was not fully activated.