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.

Poultry have higher blood glucose concentrations, which are 1.5–2 times those of their mammalian counterparts with equivalent body mass, yet do not show any adverse effects. However, the underlying mediators that inhibit systemic inflammation under hyperglycemia are unclear. In this study, chickens and rats were chosen as representatives of poultry and mammals, and the physiological differences in blood glucose regulation between them were investigated under control conditions and streptozotocin (STZ)-induced hyperglycemia, respectively, to explore the internal causes of hyperglycemia without symptoms in poultry. Firstly, the fasting blood glucose (FBG) and glucagon concentrations increased significantly (p < 0.01) and the insulin concentrations decreased when chickens and rats were treated with STZ (p < 0.001). STZ injections in rats resulted in higher oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) levels (p < 0.001), but there was no significant difference in chickens. In addition, the body weight development of STZ-inducted rats was retarded, while it was not the case for chickens receiving STZ. Secondly, high glucose metabolism products, including advanced glycation end products (AGEs) were detected in STZ-inducted rats and chickens. The AGEs concentration in the rats receiving STZ was significantly higher than that in control group rats (p < 0.001); however, there was no significant difference in chickens. Also, the concentrations of free amino acids inhibiting AGEs were further explored, and higher concentrations of taurine, leucine, and lysine were observed in chickens than those observed in rats (p < 0.05). Moreover, the concentrations were decreased significantly in STZ-treated chickens (p < 0.05). Finally, the inflammation in tissues vulnerable to high blood glucose was examined, and it was found that there were significantly increased mRNA and protein expression levels of inflammatory factors such as nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) in STZ-injected rats (p < 0.001), while there was no obvious effect in STZ-induced chickens. The results revealed the damage and inflammation resulting from STZ-induced hyperglycemia in chickens were significantly lower compared to rats. This may be attributed to the high concentrations of free amino acids in chickens, which inhibit AGE formation by functioning as carbonyl scavengers. This study elucidates the underlying causes of the absence of inflammation in chickens compared to rats under hyperglycemic conditions, offering new insights for controlling diabetic complications.

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.

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.

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.