Studies have demonstrated significant alterations in ovarian oxidative stress levels, ovarian degeneration, and follicular atresia during the broody period in geese. The results of this study showed that during the broody period, geese exhibited degraded ovarian tissues, disrupted follicular development, a thinner granulosa cell layer, and lower levels of ovarian hormones E2, P4, and AMH. Antioxidant activity (GSH, CAT, SOD, T-AOC, and the content of H2O2) and the mRNA expression levels of antioxidant genes (GPX, SOD-1, SOD-2, CAT, COX-2, and Hsp70) were significantly higher in pre-broody geese compared to laying geese, while the expression of apoptosis-related genes (p53, Caspase-3, and Caspase-9) increased and the anti-apoptotic gene Bcl-2 decreased. Additionally, proteomic analysis identified 703 differentially expressed proteins (DEPs), primarily concentrated in the GO categories of the biological process (biological regulation, response to stimulus, etc.) and enriched in the KEGG pathways (PI3K-Akt signaling pathway, etc.). Among them, XDH was central to the regulatory network. Furthermore, Western blotting revealed higher expression of XDH in the ovaries of pre-broody geese than those of laying geese. Pearson correlation analysis indicated a significant correlation between XDH expression and oxidative stress markers in the ovaries of geese (r > 0.75). Overall, these results demonstrated that geese experience ovarian atrophy and remarkably increased oxidative stress during the broody period, suggesting that XDH may be a key driver of broodiness in geese.

Feather pecking can influence the welfare and health concerns of all farmed poultry and affect production and economic aspects. Although some information is available about feather pecking behavior in chickens and ducks, the risk factors of feather pecking in goslings have not been fully demonstrated. In this study, 3-day-old Yangzhou goslings were chosen, and risk factors of feather pecking injurious behavior were investigated, including stocking density, rearing method, flock uniformity, and environmental enrichment. The gosling performed three different pecking behaviors in starter barns from 3d of age to 10d, including gentle feather pecking (GFP), severe feather pecking (SFP), and aggressive pecking (AGP), and the corresponding proportions were 82.16%, 17.02%, and 0.82%, respectively, with peak aggressive feather pecking at 4-5 days of age. The pecked gosling also led to further pecking by conspecifics. Goslings preferred to peck the back (77.32%) and head (11.14%), which caused skin damage to the epidermal and dermal layers, accompanied by a decrease in feather follicle number and diameter. In addition, the effect of the stocking density and population uniformity on the occurrence of feather pecking was determined. The higher feather pecking frequencies and poorer feather quality of goslings were observed under high-density conditions than those of lower-density environments. Importantly, the lower population uniformity resulted in more aggressive pecking, potentially linked to the establishment of a social hierarchy. Finally, environment-related changes in pecking behavior were investigated. The results showed that damp and dirty housing conditions deteriorated plumage conditions and the occurrence of feather pecking, and environment enrichment (the grass section) could significantly reduce the incidence of pecking. Taken together, lower stocking density, higher population uniformity, and the provision of enrichment can reduce the prevalence of feather pecking. Meanwhile, feather pecking in goslings, with the back being the most commonly targeted area, can lead to the loss of back feathers and even skin damage. These results help to develop effective management and prevention strategies to reduce the negative effects of pecking behavior on goose health and performance.

T-2 toxin, the most toxic type A trichothecene, is widely present in grain and animal feed, causing growth retardation and tissue damage in poultry. Geese are more sensitive to T-2 toxin than chickens and ducks. Although T-2 toxin has been reported to cause tibial growth plate (TGP) chondrodysplasia in chickens, tibial damage caused by T-2 toxin in geese has not been fully demonstrated. This study aims to investigate the adverse effects of T-2 toxin on tibial bone development, bone quality, chondrocyte differentiation, and bone metabolism. Here, forty-eight one-day-old male Yangzhou goslings were randomly divided into four groups and daily gavaged with T-2 toxin at concentrations of 0, 0.5, 1.0, and 2.0 mg/kg body weight for 21 days, respectively. The development of gosling body weight and size was determined by weighing and taking body measurements after exposure to different concentrations of T-2 toxin. Changes in tibial development and bone characteristics were determined by radiographic examination, phenotypic measurements, and bone quality and composition analyses. Chondrocyte differentiation in TGP and bone metabolism was characterized by cell morphology, tissue gene-specific expression, and serum marker levels. Results showed that T-2 toxin treatment resulted in a lower weight, volume, length, middle width, and middle circumference of the tibia in a dose-dependent manner (p < 0.05). Moreover, decreased bone-breaking strength, bone mineral density, and contents of ash, Ca, and P in the tibia were observed in T-2 toxin-challenged goslings (p < 0.05). In addition, T-2 toxin not only reduced TGP height (p < 0.05) but also induced TGP chondrocytes to be disorganized with reduced numbers and indistinct borders. As expected, the apoptosis-related genes (CASP9 and CASP3) were significantly up-regulated in chondrocytes challenged by T-2 toxin with a dose dependence, while cell differentiation and maturation-related genes (BMP6, BMP7, SOX9, and RUNX2) were down-regulated (p < 0.05). Considering bone metabolism, T-2 toxin dose-dependently and significantly induced a decreased number of osteoblasts and an increased number of osteoclasts in the tibia, with inhibited patterns of osteogenesis-related genes and enzymes and increased patterns of osteoclast-related genes and enzymes (p < 0.05). Similarly, the serum Ca and P concentrations and parathyroid hormone, calcitonin, and 1, 25-dihydroxycholecalciferol levels decreased under T-2 toxin exposure (p < 0.05). In summary, 2.0 mg/kg T-2 toxin significantly inhibited tibia weight, length, width, and circumference, as well as decreased bone-breaking strength, density, and composition (ash, calcium, and phosphorus) in 21-day-old goslings compared to the control and lower dose groups. Chondrocyte differentiation in TGP was delayed by 2.0 mg/kg T-2 toxin owing to cell apoptosis. In addition, 2.0 mg/kg T-2 toxin promoted bone resorption and inhibited osteogenesis in cellular morphology, gene expression, and hormonal modulation patterns. Thus, T-2 toxin significantly inhibited tibial growth and development with a dose dependence, accompanied by decreased bone geometry parameters and properties, hindered chondrocyte differentiation, and imbalanced bone metabolism.

A floor egg is an egg that is not laid in the nest, which is a prevalent issue in many fowl breeder farms, lowering egg collection efficiency, hatching performance, and economic benefits. Although the pattern and influencing factors of floor laying have been extensively reported in chickens and ducks, it is not clear in geese. Herein, the Yangzhou goose breeders were selected, and the time and location preferences, genetic and environmental influences, and physiological indexes in floor laying were investigated. The results revealed distinct time and location preferences existed. More floor eggs were laid from 2:00 to 5:00 and 8:00 to 12:00 am, with a concentration observed in the feed trough. Moreover, the proportion of floor eggs was higher at the early stage than at other stages of the laying cycle, and the fast-growing line laid more floor eggs than dual-purpose and high-yielding lines (P < 0.05). In addition to genetic factors, the effect of environmental influences on floor eggs was also surveyed. More floor eggs were observed in the family housing system than in large-group and small-population housing systems, and geese who reared in north-facing houses laid more floor eggs than in south-facing houses (P < 0.05). Physiological indexes were compared between floor-laying and nest-laying geese. Significantly decreased serum progesterone and prolactin levels were detected, alongside down-regulated gene expressions of progesterone receptor in ovaries, oxytocin receptor in both pituitary and ovaries, corticotropin-releasing hormone in ovaries, and dopamine receptor D2 in hypothalamus and ovaries in floor-laying geese compared to nest-laying geese (P < 0.05). In addition, a practical and inexpensive approach of adding a single decoy egg to the nest box effectively reduced the proportion of floor eggs (P < 0.05). Taken together, these data provide scientific information for patterns, genetic and environmental influences, and physiological indexes of floor eggs, thereby contributing to effective control of floor laying in goose breeders' production.

The photoperiod is the predominant environmental factor that governs seasonal reproduction in animals; however, the underlying molecular regulatory mechanism has yet to be fully elucidated. Herein, Yangzhou geese (Anser cygnoides) were selected at the spring equinox (SE), summer solstice (SS), autumn equinox (AE), and winter solstice (WS), and the regulation of seasonal reproduction via the light-driven cyclical secretion of pineal melatonin was investigated. We show that there were seasonal variations in the laying rate and GSI, while the ovarian area decreased 1.5-fold from the SS to the AE. Moreover, not only did the weight and volume of the pineal gland increase with a shortened photoperiod, but the secretory activity was also enhanced. Notably, tissue distribution further revealed seasonal oscillations in melatonin receptors (Mtnrs) in the pineal gland and the hypothalamus–pituitary–gonadal (HPG) axis. The immunohistochemical staining indicated higher Mtnr levels due to the shortened photoperiod. Furthermore, the upregulation of aralkylamine N-acetyltransferase (Aanat) was observed from the SS to the AE, concurrently resulting in a downregulation of the gonadotrophin-releasing hormone (GnRH) and gonadotropins (GtHs). This trend was also evident in the secretion of hormones. These data indicate that melatonin secretion during specific seasons is indicative of alterations in the photoperiod, thereby allowing for insight into the neuroendocrine regulation of reproduction via an intrinsic molecular depiction of external photoperiodic variations.

Circadian rhythms affect the physiology and behavior of most organisms. The ovulation–laying cycle of poultry exhibits evident rhythmic patterns. However, the underlying biological mechanism has remained unclear. Herein, Yangzhou goose (Anser cygnoides) were selected at 6:00, 12:00, 18:00, and 24:00 (n = 6/timepoint) to investigate the regulation of circadian egg-laying through the light-driven melatonin secretion. Our study revealed that the laying rates displayed diurnal fluctuations, with a peak of 40% of eggs being laid between 4:00 and 7:00. The cosine analysis revealed that the expression of clock genes exhibited rhythmicities (p < 0.05). Relevantly, melatonin secretion also displayed circadian rhythmicity and sharply decreases with increasing amount of light (p < 0.001). The immunohistochemical analysis found that the melatonin receptor is highly expressed during the night period. Notably, tissue distribution analysis further revealed that the melatonin receptor genes showed a decreasing trend in the pineal gland and hypothalamic–pituitary–gonad (HPG) axis throughout the day. Concomitantly, the expression of reproduction-related genes at 12:00 was significantly higher than that at 24:00 (p < 0.01). Taken together, these data suggested cyclical secretion of melatonin in response to photoperiod, which acts as a neuroendocrine transducer of circadian rhythm and the time preference of reproduction in domestic geese.

T-2 toxin is a dangerous natural pollutant and widely exists in animal feed, often causing toxic damage to poultry, such as slow growth and development, immunosuppression, and death. Although geese are considered the most sensitive poultry to T-2 toxin, the exact damage caused by T-2 toxin to geese is elusive. In the present study, a total of forty two 1-day-old healthy Yangzhou male goslings were randomly allotted seven diets contaminated with 0, 0.2, 0.4, 0.6, 0.8, 1.0, or 2.0 mg/kg T-2 toxin for 21 d, and the effects of T-2 toxin exposure on growth performance, feather quality, tibia development, and blood parameters were investigated. The results showed that T-2 toxin exposure significantly inhibited feed intake, body weight gain, shank length growth, and organ development (e.g., ileum, cecum, liver, spleen, bursa, and tibia) in a dose-dependent manner. In addition, the more serious feathering abnormalities and feather damage were observed in goslings exposed to a high dose of T-2 toxin (0.8, 1.0, and 2.0 mg/kg), which were mainly sparsely covered with short, dry, rough, curly, and gloss-free feathers on the back. We also found that hypertrophic chondrocytes of the tibial growth plate exhibited abnormal morphology and nuclear consolidation or loss, accompanied by necrosis and excessive apoptosis under 2.0 mg/kg T-2 toxin exposure. Moreover, 2.0 mg/kg T-2 toxin exposure triggered erythropenia, thrombocytosis, alanine aminotransferase, and aspartate aminotransferase activity, as well as high blood urea nitrogen, uric acid, and lactic dehydrogenase levels. Collectively, these data indicate that T-2 toxin had an adverse effect on the growth performance, feather quality, and tibia development, and caused liver and kidney damage and abnormal blood parameters in Yangzhou goslings, providing crucial information toward the prevention and control of T-2 toxin contamination in poultry feed.

This study was conducted to investigate the effects of different free-range systems on the growth performance, carcass traits, and meat quality of geese. Grass pasture zones in the study area were selected, and 28 d-old male Yangzhou geese with similar body weights (1.57 +/- 0.12 kg) were randomly allocated to one of three conditions: (A) free-range conditions in the apron area during 9:00 a.m.-4:00 p.m. (10-20 m from shed with grass pasture); (B) free-range conditions in the outer range from 9:00 a.m. to 4:00 p.m. (beyond 50 m from shed with grass pasture); and (C) barn system. Free range-reared geese had higher weight gain after 42 days of age than barn-reared geese, regardless of the range area. A lower feed conversion ratio was found in outer range-reared and apron area-reared geese from 28 to 63 days of age. In addition, the highest percentages of leg and breast muscle weights were observed in outer range-reared and apron area-reared geese, respectively. Finally, outer-range rearing resulted in a lower pH and lower moisture content. Therefore, these data suggest that the outer range system benefits growth performance and feed conversion ratio of geese and results in a higher percentage of leg muscle weight, lower pH, and lower moisture content.

To explore the relationship between ITGB1 gene and goose fatty liver formation, thirty healthy 70-day-old male Landes geese were randomly divided into a control group and an overfed group for 24 days of overfeeding. The sequence of ITGB1 gene was used for bioinformatics analysis, and its expression levels in the liver of geese at different overfeeding stages (12 and 24 days) were measured by RT-qPCR. Meanwhile, different doses of fatty liver formation related factors (insulin, glucose, oleic acid, linoleic acid, and palmitic acid) were used to treat goose primary hepatocytes to detect the expression levels of ITGB1 gene. The results showed that the total length of CDS is 2 418 bp, encoding 805 amino acids (which is a hydrophilic protein) and the homology between goose and duck is higher than 98 %. The expression of ITGB1 gene in goose fatty liver was significantly up-regulated (P<0.05) after 12 and 24 days of overfeeding compared with the control group. And 0.5 mmol·L-1 oleic acid, linoleic acid and palmitic acid could significantly induce the up-regulated expression of ITGB1 gene in goose primary hepatocytes (P< 0.05). Moreover, 200 mmol·L-1 glucose could also extremely significantly induce the up-regulated expression of ITGB1 gene in goose primary hepatocytes (P< 0.01). Beside, 0.2 mmol·L-1 insulin could also somehow have tend to induce the up-regulated expression of ITGB1 gene (P= 0.098). The results indicated that the up-regulation of ITGB1 gene was closely related to the formation of goose fatty liver and could be induced by factors related to fatty liver formation, which suggested that up-regulation of ITGB1 gene expression may promote the formation of goose fatty liver.

Overfeeding causes severe steatosis but not inflammation in goose liver, suggesting existence of protective components. Previous studies have shown that some intestinal microbes and their metabolites damage intestinal structural integrity and function, thus causing inflammation in the development of human and mouse nonalcoholic fatty liver disease. Therefore, this study hypothesizes that intestinal structural integrity of goose is maintained during overfeeding, which may provide goose fatty liver a protective mechanism against inflammation. To test this hypothesis, 48 seventy-day-old healthy Landes male geese were overfed (as overfeeding group) or normally fed (as control group). Blood and intestine (jejunum, ileum, and cecum) samples were harvested on the 12th and 24th d of overfeeding. Data showed that goose fatty liver was successfully induced by 24 d of overfeeding. Hematoxylin-eosin staining analysis indicated that the arrangement of villi and crypts in the intestine was orderly, and the intestinal structure was intact with no pathological symptoms in the 2 groups. Enzyme-linked immunosorbent assay and quantitative PCR analysis indicated no significant differences in the expression of tight junction and inflammation-related genes as well as plasma lipopolysaccharide concentration between the groups. Ileal hypertrophy and cecal atrophy were observed in the overfed vs. control geese, probably because of change of sphingolipid metabolism. Activation of apoptotic pathway may help cecum avoid necrosis-induced inflammation. In conclusion, healthy and intact intestine provides a layer of protection for goose fatty liver against inflammation. Sphingolipid metabolism may be involved in the adaptation of ileum and cecum to overfeeding. The hypertrophy of ileum makes it an important contributor to the development of goose fatty liver. The atrophy and decline in the function of cecum may be caused by apoptosis induced by overfeeding.

为探究磷脂磷酸酶3 (PLPP3)基因与鹅肥肝形成的关系,选取30只70日龄健康朗德鹅,随机分为填饲组与对照组,采用实时荧光定量PCR技术测定朗德鹅不同填饲阶段(填饲12和24 d)肝脏、胸肌和腹脂中PLPP3基因的表达水平;利用不同剂量的脂肪肝形成相关因子(胰岛素、葡萄糖、油酸、亚油酸和棕榈酸)分别处理朗德鹅原代肝细胞,检测这些因子对PLPP3基因表达的影响.结果 表明:与对照组相比,填饲12 d时,肝脏、腹脂和胸肌中PLPP3基因的表达均显著或极显著下调;填饲24 d时,肝脏中表达差异不显著,腹脂中极显著下调,胸肌中显著上调;在鹅原代肝细胞中,与对照组相比,处理组葡萄糖、棕榈酸和油酸能显著抑制PLPP3基因的表达,而胰岛素和亚油酸处理则无显著效应.这一研究提示PLPP3基因的表达变化与鹅肥肝形成密切相关,且受脂肪形成相关因子的调控,说明PLPP3可能在鹅肥肝形成中有重要作用.

本试验旨在研究在低蛋白水平日粮中添加蛋白酶对肉鸭生长和屠宰性能的影响.试验选取7日龄体重相近的樱桃谷肉鸭360羽,随机分为A、B、C三个组,每组3个重复,每个重复40羽鸭(公、母各半),试验期42 d.A组为对照组,B组和C组的日粮蛋白水平分别为对照组的95％和92％,并在这两组日粮中分别添加0.125％的蛋白酶.所得的试验数据表明在肉鸭日粮中添加蛋白酶可以提高肉鸭平均日增重和体重,并可降低料重比,且在95％蛋白水平达到显著水平(P<0.05).因此,在肉鸭日粮中添加0.125％的蛋白酶可以适当降低饲料蛋白水平而不会影响其生产性能,且以降低5％时为宜.