An experiment was conducted using a total of 540 one-day-old Yangzhou geese to study the effect of rearing system on growth performance, carcass trai

We investigated the effects of dietary fiber on growth performance, slaughter performance, serum biochemical parameters, and nutrient utilization in geese. A total of 468 one-day-old healthy male Yangzhou goslings with similar body weight were randomly divided into 3 groups with 6 replicates per group and 26 geese per replicate. The geese were then raised for 70 days on diets with a dietary fiber level of 2.5% (Group I), 6.1% (Group III), or 4.3% for d one to 28 and 6.1% for d 29 to 70 (Group II). The geese in Groups II and III had higher body weight, higher average daily gain, and lower ratio of feed to gain compared with those in Group I (P < 0.05 for each comparison). The geese in Groups II and III had greater body-size measurements (half-diving length, body length, keel length, and shank circumference), heavier viscera (heart, gizzard, proventriculus, duodenum, jejunum, ileum, and cecum), greater slaughter yield (semi-eviscerated carcass yield, eviscerated carcass yield, and breast yield), lower serum levels of alanine transaminase, uric acid, and blood urea nitrogen, and higher serum levels of glucose and high-density lipoprotein compared with those in Group I (P < 0.05 for each comparison). The geese in Groups II and III exhibited greater utilization of energy and crude protein compared with those in Group I (P < 0.05). Taken together, the results suggest that the low-fiber diet had negative effects on growth performance, slaughter performance, serum biochemical parameters, and nutrient utilization. As herbivorous poultry, geese depend on dietary fiber for normal performance. Dietary fiber is thus an essential nutrient for geese.

Aflatoxin B₁ (AFB₁) is the predominant mycotoxin that originated toxicity in broilers through oxidative damage, intestinal barrier dysfunction, reduced immune system and dysfunction of microorganisms and enzymes in target organs. The intestine is the first AFB₁ target organ destroyed after the bird's body is induced. This review summarises the current knowledge of the negative results of AFB₁‐induced intestinal damage on broiler production. It was conducted in accordance with the relevant studies in the cited literatures being retrieved from PubMed, Google Scholar, Science Direct and Web of Science. First, AFB₁ can change the intestinal barrier function by destroying the intestinal architecture, tissue and cell integrity of the gut epithelium. Second, AFB₁ can damage the immune barrier function of the gastrointestinal mucosa. Third, the microbiota of birds interacts closely with the ingested aflatoxin. Finally, because broilers are tremendously sensitive to AFB₁ contamination, the poisonous and noxious effects of this mycotoxin in the broiler industry cause millions of dollars in losses every year. This review briefly discussed that the AFB₁, which affects the intestines of broiler chickens, was reduced the immune apparatus, antioxidant protection system, gastric system, and broiler production status and its impact on human health. Therefore, this review will improve our perception of the important intestine in a bird's health and the adverse effect of AFB₁.

Objective: The present study was conducted to investigate the effects of lycopene on growth performance, abdominal fat deposition, serum lipids levels, activities of hepatic lipid metabolism related enzymes and genes expression in broiler chickens.Methods: A total of 256 healthy one-day-old male Arbor Acres broiler chicks were randomly divided into four groups with eight replicates of eight birds each. Birds were fed basal diet supplemented with 0 (control), 100, 200, and 400 mg/kg lycopene, respectively.Results: Dietary 100 mg/kg lycopene increased the body weight at 21 day of age compared to the control group (p<0.05). Compared to the basal diet, broilers fed diet with 100 mg/kg lycopene had decreased abdominal fat weight, and broilers fed diet with 100 and 200 mg/kg lycopene had decreased abdominal fat percentage (p<0.05). Compared to control, diets with 100, 200, and 400 mg/kg lycopene reduced the levels of total triglyceride and total cholesterol in serum, and diets with 100 and 200 mg/kg lycopene reduced the level of serum low density lipoprotein cholesterol (p<0.05). The activity of fatty acid synthase (FAS) in 400 mg/kg lycopene treated broilers and the activity of acetyl-CoA carboxylase (ACC) in 100, 200, and 400 mg/kg lycopene treated broilers were lower than those fed basal diet (p<0.05). Lycopene increased the mRNA abundance of adenosine monophosphate activated protein kinase α (AMPK-α), whereas decreased the mRNA abundance of sterol regulatory elementbinding protein 1, FAS, and ACC compared to the control group (p<0.05).Conclusion: Dietary lycopene supplementation can alleviate abdominal fat deposition and decrease serum lipids levels, possibly through activating the AMPK signaling pathway, thereby regulating lipid metabolism such as lipogenesis. Therefore, lycopene or lycopenerich plant materials might be added to poultry feed to regulate lipid metabolism.

The present study aims to evaluate the effects of lycopene (LYC) supplementation on the intestinal immune function, barrier function, and antioxidant capacity of broilers fed with aflatoxinB1 (AFB₁) contaminated diet. A total of 144 one-day-old male Arbor Acres broilers were randomly divided into three dietary treatment groups; each group consisted of six replicates (eight birds in each cage). Treatments were: (1) a basal diet containing neither AFB₁ nor LYC (Control), (2) basal diet containing 100 µg/kg AFB₁, and (3) basal diets with 100 µg/kg AFB₁ and 200 mg/kg LYC (AFB₁ and LYC). The results showed that dietary LYC supplementation ameliorated the AFB₁ induced broiler intestinal changes by decreasing the inflammatory cytokines interferon-γ (IFN-γ), interleukin 1beta (IL-1β), and increasing mRNA abundances of cludin-1 (CLDN-1) and zonula occludens-1 (ZO-1) in the jejunum mucosa. On the other hand, AFB₁-induced increases in serum diamine oxidase (DAO) activities, D-lactate concentration, mucosal malondialdehyde (MDA), and hydrogen peroxide (H₂O₂) concentrations were reversed by dietary LYC supplementation (p < 0.05). Additionally, LYC supplementation ameliorated the redox balance through increasing the antioxidant enzyme activities and their related mRNA expression abundances compared to AFB₁ exposed broilers. In conclusion, dietary supplementation with LYC could alleviate AFB₁ induced broiler intestinal immune function and barrier function damage and improve antioxidants status.

This study was conducted to investigate the effects of lycopene (LYC) on mitochondrial oxidative injury and dysfunction in the liver of aflatoxin B₁ (AFB₁)-exposed broilers. A total of 192 healthy 1-day-old male broilers were randomly divided into 3 groups with 8 replicates of 8 birds each. Birds in the 3 groups were fed basal diet (control), basal diet with 100 µg/kg AFB₁, and basal diet with 100 µg/kg AFB₁ and 200 mg/kg LYC, respectively. The experiment lasted 42 d. The results showed that AFB₁ decreased average daily body weight gain (ADG), average daily feed intake, and gain to feed ratio (G :F) compared to the control group, the LYC supplementation increased ADG and G/F compared to AFB₁ group (P < 0.05). Broilers in the AFB₁ group had lower mitochondrial glutathione (mGSH) concentration and glutathione peroxidase (GSH-Px), manganese superoxide dismutase (MnSOD), and thioredoxin reductase activities, and higher hydrogen peroxide (H₂O₂) and reactive oxygen species (ROS) concentrations than the control group (P < 0.05). The LYC increased mGSH concentration and GSH-Px and MnSOD activities, and decreased H₂O₂ and ROS concentrations compared to AFB₁ group (P < 0.05). Broilers fed the AFB₁ diet showed increased mitochondrial swelling and decreased adenosine triphosphate concentration than the control group, and LYC had opposite effects (P < 0.05). The AFB₁ decreased the activities of mitochondrial electron transfer chain (ETC) complexes I, II, III, and V, downregulated the mRNA expression levels of hepatic MnSOD, thioredoxin 2, thioredoxin reductase, peroxiredoxin-3, peroxisome proliferator-activated receptor γ coactivator 1α, nuclear respiratory factor 1, and mitochondrial transcription factor A compared with the control group (P < 0.05), and LYC increased activities of mitochondrial ETC complexes III and V, and upregulated mRNA expression levels of these genes in comparison to AFB₁ group (P < 0.05). In conclusion, the LYC protected broilers from AFB₁-induced liver mitochondrial oxidative injury and dysfunction by stimulating mitochondrial antioxidant capacity and maintaining mitochondrial biogenesis.