Muscle, the largest tissue in geese, is crucial for developing goose fatty liver. Investigating the influence of Insulin-like Growth Factor Binding Protein 2 (IGFBP2) on muscle during fatty liver development is crucial for understanding its regulatory mechanisms. In this study, twenty-four 70-day-old male Landes geese were divided into two groups: an overfeeding group and a control group (n = 12 each). Pectoral muscle samples were collected at 82 and 94 days of age. Additionally, twenty-four 10-day-old geese were divided into a glucose injection group and a saline control group (n = 12 each), with pectoral muscle samples collected 2 hours post-injection at 17 days of age. Goose primary myocytes were treated with glucose (0, 25, 50, and 100 mmol/L) or insulin (0, 5, 10, and 20 nmol/L) and transfected with an IGFBP2 overexpression vector or an empty vector. Results demonstrated that overfeeding, glucose injection, 50 and 200 mmol/L glucose treatment, and 10 and 20 nmol/L insulin treatment significantly inhibited the expression of IGFBP2 in both muscle and cell samples (P < 0.05). Overexpression of IGFBP2 increased the expression of LOC106030908, FGB, and LOC106040417, while inhibiting PLPP4, PTGS2, IL6, and LOC106041919 (P < 0.05). Notably, gene expression showed an inverse pattern in the muscles of overfed geese. Additionally, glucose and insulin upregulated LOC106041919 and LOC106040417 while downregulating LOC106030908 in goose myocytes (P < 0.05). These results suggest that glucose and insulin modulate inflammation and glycolipid metabolism genes in goose muscle via IGFBP2 during fatty liver development, providing new molecular insights.

Fatty liver disease represents a major metabolic disorder affecting domestic animals worldwide, with significant implications for animal health, welfare, and agricultural productivity. Disrupted communication between mitochondria and other organelles-particularly the endoplasmic reticulum, lipid droplets, and lysosomes-plays a critical role in disease pathogenesis. This review synthesizes knowledge on inter-organellar communication across domestic animals, with emphasis on species-specific adaptations. We address the "Dairy Cow Paradox"-periparturient dairy cows develop severe hepatic steatosis (>30% liver fat), yet under sterile conditions, they have a higher threshold for progressing to sterile steatohepatitis compared to rodents and humans. However, it is critical to note that severe fatty liver in dairy cows is indeed associated with impaired autophagy, inflammation, and liver damage, particularly when accompanied by ketosis or concurrent infections, and 39% of transition cows exhibit moderate to severe lymphocytic hepatitis. We propose that the tolerance to severe steatosis in dairy cows arises from three adaptations: (1) attenuated innate immune sensing via the cGAS-STING pathway; (2) enhanced lipid buffering from perilipin 5 (PLIN5) with a hypothesized ruminant-specific Val152 substitution that may stabilize lipid droplet-mitochondria contacts; and (3) dampened calcium signaling due to ER-mitochondria membrane lipid raft rigidity, elevated inositol 1,4,5-trisphosphate receptor 2 (IP3R2) expression, and reduced mitochondrial calcium uniporter (MCU) conductance. We contrast this with the inflammatory steatohepatitis common in rodent models driven by calcium overload and mitochondrial DNA (mtDNA) release, and glucocorticoid-mediated mitofusin 1 (MFN1) suppression, causing mitochondrial fragmentation in poultry. We identify critical knowledge gaps, including the need to define bovine and avian mitochondria-associated endoplasmic reticulum membrane (MAM) proteomes and spatially resolve hepatic zonal communication patterns. Targeting organellar communication hubs with nutraceuticals or pharmacological agents offers promising therapeutic strategies.

The liver of geese has a strong ability to deposit fat and also has the ability to resist inflammation. Goose fatty liver represents a unique physiological model that exhibits no or low-level inflammation despite severe steatosis. Mitochondria and their proteins play a crucial role in the regulation of hepatic inflammation. However, it remains unclear whether choline dehydrogenase (CHDH), a mitochondrial protein, is involved in fat deposition and inflammation resistance in goose fatty liver formation. Here, we observed distinct expression patterns of mitochondrial CHDH (mCHDH) other than global CHDH (gCHDH) in goose versus mouse fatty livers, highlighting the unique role of mCHDH in goose fatty liver formation. Overexpression of gCHDH in goose primary hepatocytes led to increased cellular lipid accumulation, mitochondrial membrane potential (MMP) and respiratory chain complex II activity, alongside activation of immune response, apoptosis, cell adhesion, and lipid metabolism-related pathways. Moreover, overexpression studies in HepG2 cells revealed that both gCHDH and a mitochondrial targeting sequence-mutant CHDH (Δ1-38CHDH) elevated MMP, but they differentially regulated reactive oxygen species (ROS) level (Δ1-38CHDH slightly reduced intracellular ROS level) and the abundance of mitochondria-related proteins (gCHDH selectively increased tAMPK and decreased LC3B in mitochondrial lysates, whereas Δ1-38CHDH mainly reduced tAMPK and pAMPK in whole-cell lysates). Furthermore, transcriptome sequencing and mass spectrometry analyses revealed that CHDH may participate in processes such as immune response, ubiquitin-mediated degradation, autophagy, signal transduction and lipid metabolism. In summary, gCHDH and mCHDH contribute to the formation of goose fatty liver by affecting mitochondrial protein composition (AMPK, LC3B), mitochondrial function and related biological processes, though their effects exhibit certain differences. These findings provide new insights into the mechanism underlying the uniqueness of goose fatty liver.

Chicken somatic cells exhibit cell autonomous sex identity (CASI), where sexual features are determined by sex chromosomes rather than hormones. CASI arises from sex‑biased gene expression due to lack of dosage compensation on sex chromosomes. To identify CASI‑determining genes (CASIDGs), we analyzed transcriptomes of wattles (phenotypically hormone‑sensitive) and pectoral muscles (phenotypically hormone‑unresponsive) from 6‑week‑old roosters and hens, with or without sex hormone treatment. Inter‑sex differentially expressed genes (DEGs) mainly located on the Z chromosome and autosomes 1‑2, while hormone‑affected DEGs predominantly on autosomes 1‑3. After removing hormone‑affected DEGs from the inter‑sex DEGs, 285 DEGs (51.23% on sex chromosome) remained for pectoral muscle, and 255 DEGs (63.93% on sex chromosome) for wattle. Out of the 89 DEGs shared by these two tissues, 88 were located on sex chromosomes and were considered candidate CASIDGs. These candidate CASIDGs were mainly enriched in mitochondrial protein synthesis and isomerase activity-related pathways. Among the CASIDGs, HINT1 and MED18 were validated according to the screening criteria. Overexpressing these two genes in primary muscle cells could affect immune/inflammatory responses, cell proliferation and migration, cytoskeleton, and extracellular matrix interactions. Additionally, 139 autosomal DEGs for pectoral muscle and 92 for wattle were identified as candidate sex marker genes. Among these, IRF9 and CCL4 were co‑regulated by HINT1 and MED18. In conclusion, the sex characteristics of chicken somatic cells reflect the combined effects of CASIDGs and sex hormones. HINT1 and MED18 are confirmed as candidate CASIDGs. These findings lay a solid foundation for elucidating the CASI mechanism in avian somatic cells.

Unlike mammals, where systemic sex hormones determine somatic sexual identity, chickens primarily employ a cell-autonomous mechanism, known as the cell autonomous sexual identity (CASI) hypothesis. However, tissue sensitivity to sex hormones varies significantly. This study aimed to elucidate the specific role of the estrogen/estrogen receptor α (ERα) system in this context. We assessed protein levels of key sex hormone receptors, including ERα, estrogen receptor β (ERβ), and androgen receptor (AR), in the tissues of 6-week-old and adult chickens. Results showed that ERα protein was markedly abundant in hormone-sensitive tissues (comb and wattles) but low in insensitive ones (muscle and liver); this pattern was not observed for ERβ or AR. Functionally, in the absence of estrogen, ERα overexpression in ERα-deficient primary muscle cells affected immunity but not sexual differentiation-related pathways. In contrast, analysis on the transcriptomes of ERα-rich wattle tissues indicated that the genes differentially expressed between estrogen-treated versus untreated groups were enriched in the pathways critical for development, neuroactive ligand-receptor interaction, and glycerolipid metabolism to establish sexual phenotype. In conclusion, estrogen regulates somatic sex identity via ERα in a tissue-specific manner, with regulatory intensity dictated by local ERα abundance. This provides a crucial supplement to the CASI hypothesis.

Understanding sex determination mechanism is crucial for elucidating sexual evolution and sex control in animal husbandry. In this study, data showed that doublesex and mab-3 related transcription factor 2 (DMRT2) expression in gonads was developmentally regulated in a sex- and lateralization-specific manner. The nuclear localization signal of DMRT2 was identified, showing high expression in the female gonadal cortex. Transcriptome and chromatin immunoprecipitation followed by sequencing (ChIP-seq) analyses screened and validated target genes (component of inhibitor of nuclear factor kappa B kinase complex (CHUK) and SRY-box transcription factor 9 (SOX9)) and downstream signaling pathways (e.g., sex determination, cell apoptosis, and inflammation related). It was also validated that DMRT2 could promote cell proliferation and inhibit apoptosis. The effect of DMRT2 on apoptosis and inflammation was mediated by CHUK. These factors may potentially regulate apoptosis pathway and Wnt signaling pathway. In conclusion, DMRT2 participates in sex differentiation and development of chicken gonads by regulating proliferation, apoptosis, and inflammatory pathways through target genes such as CHUK and SOX9. The novel mechanism of DMRT2 regulating avian gonadal differentiation and development may deepen understanding of vertebrate sexual evolution and facilitate sex control in poultry.

Mitochondria are crucial carriers of maternal effects, and their function is closely related to energy metabolism and disease occurrence. Previous studies have shown that chickens with different mitochondrial haplogroups exhibit differences in production performance, but the underlying mechanism remains unclear. This study investigates the differences in mitochondrial structure and function-related indices between the A and E mitochondrial haplogroups (referred to as A-group and E-group) in recessive white-feathered chickens. It was achieved using in vivo fasting/refeeding models and an in vitro model of treating hepatocytes with nutritional factors (glucose and fatty acids). In vivo study indicated that compared to A-group chicken hepatocytes, E-group hepatocytes had shorter perimeters of mitochondria and shorter lengths of mitochondria associated with the endoplasmic reticulum membrane during refeeding (p < 0.05); mitochondria were more abundant (p = 0.05) but displayed compromised structural integrity during fasting; mitochondrial swelling was more severe during both refeeding and fasting (p < 0.01, p < 0.05); the protein level of mitofusin 2 (MFN2) was lower during fasting (p < 0.05); and there were more vacuoles and lipid accumulation in liver sections during refeeding (p < 0.05). In cultured hepatocytes, compared to A-group cells, E-group cells had higher reactive oxygen species (ROS) level after oleic acid treatments (p < 0.001); the protein level of microtubule-associated protein 1A/1B-light chain 3 beta (LC3) was lower after glucose treatment (p < 0.01), and the protein levels of MFN2 and LC3 were lower after oleic acid treatment (p < 0.01, p < 0.05). These findings suggest that mitochondrial haplogroups are associated with mitochondrial structure and function, oxidative stress, autophagy, and lipid metabolism of chicken hepatocytes in response to energy stimulation. The findings may explain how mitochondrial haplogroups affect chicken production performance.

This study investigated the impact of Clostridium butyricum, Bacillus subtilis, and the mixed probiotics on the growth, slaughter performance and antioxidant capacities of the blood, ileal mucosa and liver of Yangzhou geese. Two hundred and eighty-eight 1-day-old male Yangzhou geese were randomly assigned to four groups, including group A (fed with the basal diet), and groups CB, BS and CBS (fed with the basal diet plus 7.5 x 105 CFU/kg Clostridium butyricum, 5.0 x 106 CFU/kg Bacillus subtilis or the mixture of both bacteria, respectively). After 70 d of feeding, supplementing Clostridium butyricum, Bacillus subtilis or their mixture significantly increased body weight gain and feed intake per day, the pectoral muscle index, the antioxidant capacities of liver and ileal mucosa, and immune gene expression of ileum, and decreased apoptotic gene expression of ileum. Moreover, supplementing Clostridium butyricum significantly increased shear force of pectoral muscle and ileal glutathione S-transferase, supplementing Bacillus subtilis significantly increased ileal glutathione and total antioxidant capacity, and blood total antioxidant capacity, supplementing the bacterial mixture significantly decreased gizzard index and ileal TLR4 and MyD88 expression compared with single bacterium. In summary, supplementing probiotics was generally beneficial to the growth and slaughter performance, the ileal immune potential, the antioxidant capacity and ileal apoptosis of geese. Therefore, Clostridium butyricum, Bacillus subtilis or their mixture can be applied as feed additives to promote goose production performance and health.

All identified genes on the avian W chromosome have homologous counterparts on the Z chromosome, with protein-coding genes showing over 90% homology. These W-linked genes are typically dose-sensitive and conserved, ensuring balanced expression between sexes during development. This study explores the sequence characteristics, expression patterns, and potential functions of the RASA1 gene in chicken embryos. In gonads, RASA1-Z was found to be more highly expressed in males, but total mRNA levels (RASA1-C) were higher in females due to RASA1-W compensation. However, RASA1 protein levels were significantly higher in males, suggesting limited contribution of RASA1-W. Knockdown of RASA1-Z reduced both mRNA and protein levels, whereas overexpression of RASA1-W increased mRNA but not protein levels. Sex reversal experiments showed no significant changes in RASA1 expression, indicating it is not involved in gonadal sex differentiation. However, higher expression in the left female gonad suggests a role in gonadal development. Functional studies using CCK8 proliferation assays revealed that RASA1-Z promotes cell proliferation, while RASA1-W has minimal impact. This study indicates that RASA1 primarily functions in cell proliferation and angiogenesis rather than sex differentiation, with RASA1-W contributing to transcript balance but not protein output.

To investigate the functions of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in the goose fatty liver, a total of 30 healthy 63-day-old male Landes geese were selected and randomly assigned to control group and overfeeding group. The overexpression or RNA interference assay of PGC-1α was performed in goose primary hepatocytes. Our data showed that the PGC-1α expression was increased in fatty liver. The abundance of mitochondrial biosynthesis-related and energy metabolism-related genes, including mitochondrial transcription factor A (TFAM), mitochondrial transcription factor B1 (TFB1M), mitochondrial transcription factor B2 (TFB2M), nuclear respiratory factor 1 (NRF1), DNA topoisomerase I mitochondrial (TOP1MT), peroxisome proliferator-activated receptor gamma coactivator 1-beta (PGC-1β), sirtuin 3 (SIRT3), mitochondrially encoded cytochrome B (CYTB), and AMP-activated protein kinase alpha (AMPKα) were significantly increased in fatty liver. The abundance of TFAM, TFB1M, TFB2M, NRF1, and TOP1MT transcript was induced by PGC-1α overexpression, but inhibited by PGC-1α interference in primary hepatocytes. The mRNA expression levels of PGC-1β, SIRT3, SIRT5, CYTB, and AMPKα were significantly enhanced after PGC-1α overexpression. However, the mRNA expression levels of PGC-1β, SIRT5 and AMPKα were decreased after PGC-1α interference. Furthermore, we observed a significant increase in the mitochondrial DNA (mtDNA) copy number, the activity of mitochondrial respiratory chain complex Ⅳ (MRCC Ⅳ), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and the NAD+/NADH ratio in fatty liver. But the activity of MRCC Ⅴ, as well as the levels of ADP and ATP in fatty liver were reduced. Additionally, the mtDNA copy number, the activity of MRCC Ⅰ, MRCC Ⅲ-Ⅴ, SDH, and MDH, and NAD+/NADH ratio were enhanced by PGC-1α overexpression; Whereas the mtDNA copy number, the activity of MRCC Ⅰ, SDH, and MDH, and the ratio of NAD+/NADH were inhibited by PGC-1α interference. In conclusion, these findings suggest that PGC-1α improves mitochondrial biosynthesis and energy metabolism in goose fatty liver, which may be an adaptive mechanism for goose fatty liver to cope with steatosis.

This study was to screen, verify and apply molecular markers of candidate genes (FREM1 and PTPRM) related to eyelid defect, which may facilitate establishment of autosexing strains of Huoyan goose. Using 150 1-d-old Huoyan geese containing 100 with colobomus eyelid and 50 with normal eyelid, 6 and 3 polymorphic loci single nucleotide polymorphisms (SNPs) were identified in the 1-kb upstream sequences of FREM1 transcript 1 and transcript 2, respectively. All identified SNPs showed significant association with the colobomus eyelid trait (P < 0.05). To further investigate the regulatory effects of these SNPs, dual-luciferase reporter assays in goose primary hepatocytes and myocytes confirmed that mutations at SNP2 locus (c.-385 A > T) in transcript 1 and SNP3 locus (c.-714 A > G) in transcript 2 significantly enhanced or suppressed FREM1 expression, respectively (P < 0.05). Subsequently, bioinformatics analysis predicted that SNP2 was located within the binding sequence of Pou1f1, and that SNP3 was located within the binding sequence of CUX2. Treatment with 1 μmol/L dexamethasone (drug for Poulf1) induced FREM1 expression (P < 0.05), and treatment with 75 μg/mL rifampicin (drug for CUX2) suppressed FREM1 expression (P < 0.05). Furthermore, quantitative real-time PCR analysis revealed that female Huoyan geese with either the normal eyelid or wild type genotype exhibited significantly higher FREM1 expression in both eyelid and liver tissues of than those with the colobomus eyelid or mutant genotype, respectively (P < 0.05). Based on the key polymorphic locus in FREM1 identified in this study, combined with previously discovered key locus in PTPRM, marker-assisted selection led to an increase in the colobomus eyelid rate, reaching 97.03 % in 303 offspring. In conclusion, the findings strongly support FREM1 and PTPRM as causative genes for the colobomus eyelid trait; the obtained molecular markers can significantly improve the selection efficiency; mutations at the key SNP loci in the upstream sequences of FREM1 can alter its expression by affecting the binding affinity of the putative transcription factors, Pou1f1 and CUX2.

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is a key regulator of lipid metabolism, particularly in fatty acid oxidation and energy homeostasis. A recent study revealed that PGC-1α exhibits differential expression in mammalian and goose fatty liver, but its function in lipid accumulation in goose fatty liver remains unclear. In this study, thirty 63-day-old male Landes geese were randomly assigned to control and overfeeding groups. Histological analysis was performed using Hematoxylin and Eosin staining and Sirius Red staining after feeding. In vitro, primary goose hepatocytes were treated with lipid accumulation-inducing factors, and PGC-1α mRNA expression was measured. Overexpression and RNA interference of PGC-1α were conducted in primary hepatocytes, followed by transcriptome sequencing analysis. Differential gene expression related to lipid metabolism was analyzed in both goose liver tissue and cultured cells. Our results indicated that despite significant lipid deposition in the liver, no fibrosis was observed in goose fatty liver. PGC-1α mRNA expression was upregulated after glucose, insulin, and palmitic acid treatment (P < 0.05), with no significant changes observed after sodium oleate treatment (P > 0.05). After knocking down PGC-1α, lipid deposition occurred in cells, while overexpression of PGC-1α improved lipid accumulation. Transcriptome sequencing analysis revealed significant upregulation of genes involved in lipid metabolism in PGC-1α-overexpressing cells, particularly in pathways related to arachidonic acid metabolism, fatty acid biosynthesis, linoleic acid metabolism, and adipocytokine signaling. Key genes such as ACSS2, ACOX1, CPT1A, ACSL1 and ACADL were significantly upregulated in both PGC-1α-overexpressing cells and fatty livers from overfed geese (P < 0.05). Knockdown of PGC-1α led to a significant reduction in the mRNA levels of ACSS2, ACOX1, and CPT1A (P < 0.05). In conclusion, these findings demonstrate that PGC-1α activation enhances both fatty acid oxidation and synthesis-related pathways in goose hepatocytes, thereby facilitating lipid turnover and reducing excessive lipid accumulation. This “dual-regulatory” role may represent a unique adaptive mechanism by which geese mitigate hepatic steatosis without triggering inflammation or fibrosis.

Goose fatty liver, a product of short-term overfeeding, is notable for its high nutritional value and unique tolerance to severe steatosis without inflammation, in contrast to human nonalcoholic fatty liver disease (NAFLD). It is known that choline can alleviate nonalcoholic steatohepatitis and liver cirrhosis, inhibit cell apoptosis, promote lecithin synthesis and fat transportation out of the liver, and relieve cardiovascular disease-related symptoms (e.g., hyperlipidemia and hypercholesterolemia). This study investigates the role of Proline Rich Membrane Anchor 1 (PRIMA1) in inhibiting inflammation through choline metabolism during goose fatty liver formation. Overfeeding of geese resulted in increased body and liver weights, elevated fat content, and significantly higher expression of PRIMA1, accompanied by decreased LITAF and CRP (important pro-inflammatory cytokines) expression and reduced acetylcholinesterase (AchE) activity, which was assessed by the amount of produced choline. The overexpression of PRIMA1 in goose primary hepatocytes (GPHs) enhanced AchE activity. Consistently, glucose-induced upregulation of PRIMA1 expression in GPHs was accompanied by increased AchE activity. Further combined treatment with glucose and PRIMA1 knockdown in GPHs showed that downregulation of PRIMA1 attenuated the suppression of LITAF and CRP expression caused by glucose addition, but had no effect on the rise in AchE activity. These findings indicate that PRIMA1 may play a role in promoting choline metabolism and protecting against liver inflammation, offering insights into potential therapeutic targets for NAFLD.

As mitochondria play an important role in nutritional/energy metabolism, nutritional disturbances may affect animal growth, development and performance through modulating mitochondrial structure and function. This study aimed to elucidate the effects of nutritional disturbances on mitochondrial structure and function, oxidative stress, and fat deposition in the hepatocytes of chickens with A or E mitochondrial haplogroups (referred to as A-group and E-group). For in vivo experiments, white-feathered broiler chickens were fasted for 12 h or refed for 2 h after 10 h fasting. For in vitro experiments, chicken embryonic primary hepatocytes were treated with 50 mmol/L glucose or 0.25 mmol/L oleic acid. Data indicated that compared to fasted chickens, fat content (p < 0.01), the number of aggregated ribosomes (p < 0.05), and mitochondrial membrane potential (p < 0.05) were increased in the refed chickens of both haplogroups. However, the number of mitochondria was reduced (p < 0.01) and ROS level was increased (p < 0.05) in the refed E-group chickens, and the protein levels of MFN2 and SOD2 were reduced (p < 0.05) in the refed A-group chickens. Moreover, compared to the control cells, triglyceride content was increased in the cells of both haplogroups (p < 0.01), ROS level was reduced in the E-group cells (p < 0.01), and mitochondrial membrane potential was reduced (p < 0.05) and CYTB protein content was increased (p < 0.05) in the A-group cells after treatment with oleic acid. In addition, mitochondrial membrane potential was increased in the A-group cells after treatment with glucose (p < 0.01). These results indicate that nutritional disturbances affected fat deposition, mitochondrial membrane potential, the number of aggregated ribosomes, and ROS level in chicken liver cells. Moreover, ROS level, mitochondrial number, mitochondrial membrane potential, and the abundance of certain mitochondrial proteins were different between the A- and E-groups or between glucose and oleic acid treatments. These findings provide references for improving animal physiological functions and production performance by adjusting nutritional levels.

Background: While the mechanism of asymmetric gonadal development is generally understood, the mechanism of asymmetric oviduct development remains unclear. Methods: Right and left oviducts were collected from chick embryos at three developmental stages (Embryonic day 7.5, E9.5, and E11.5) for RNA-seq analysis (RNA-seq). Whole-genome resequencing (WGRS) was performed on hens with bilateral reproductive systems (a rare natural occurrence) and unilateral controls. These data were co-analyzed with public RNA-seq data of female embryonic gonads at different developmental stages (E4.5, E5.5, and E6.5) to screen for candidate genes affecting oviduct degeneration/development. Results: RNA-seq analyses showed that a total of 27, 10, and 38 DEGs were identified between the left and right oviducts at E7.5, E9.5, and E11.5, respectively. WGRS analyses revealed 1045 differentially mutated genes (DMGs) between bilateral (D) and unilateral (S) groups. Preliminary validation highlighted BMP7, PAK3, SLC6A11, PITX2, and SMC1B as candidate genes influencing oviduct asymmetry. Conclusions: This study provides insights into the genetic basis of asymmetric oviduct development and lays the groundwork for breeding hens with bilateral reproductive systems.

Protein Kinase A (PKA) is found in a wide range of body tissues and is involved in various cellular activities. PKA has been observed to interact with key proteins in the nuclear factor kappa-B (NF-κB) pathway to activate the pathway, thereby triggering an inflammatory response. However, the role of PKA in the anti-inflammatory mechanism of goose fatty liver remains to be elucidated. A total of 16 healthy 70-day-old male Lander geese were randomly divided into the control and overfeeding groups. Next, goose primary hepatocytes were treated with 200 mmol/L glucose. The protein levels of p-IκB, PKA and tumor necrosis factor alpha (TNFα) in the liver and hepatocytes, as well as the interaction of p-IκB and PKA were detected. Finally, the hepatocytes were treated with a combination of 200 mmol/L glucose and overexpressed or knocked-down PKA. The protein levels of p-IκB, PKA and TNFα were measured. The results showed that the levels of p-IκB, PKA and TNFα were significantly reduced (P < 0.05) in goose fatty liver compared to normal liver, and the interaction of p-IκB and PKA was inhibited in overfeeding group. The levels of p-IκB and PKA in 200 mmol/L glucose-treated hepatocytes were significantly reduced compared with control group (P < 0.05). Furthermore, the level of TNFα was unchanged (P > 0.05), and the interaction of p-IκB and PKA was inhibited in 200 mmol/L glucose-treated hepatocytes. The levels of p-IκB, PKA, and TNFα were significantly increased in the hepatocytes overexpressing PKA and treated with 200 mmol/L glucose compared to control group (P < 0.05). In contrast, the levels of p-IκB, PKA, and TNFα were significantly suppressed in the knockdown of PKA and treated with 200 mmol/L glucose compared with control group (P < 0.05). In conclusion, inflammation was suppressed in both the goose fatty liver and the hepatocytes treated with 200 mmol/L glucose. In addition, glucose inhibits inflammation in goose fatty liver by reducing the interaction between PKA and IκB.

Non-alcoholic fatty liver disease (NAFLD) has emerged as a significant metabolic disorder in modern poultry production, particularly affecting high-yielding laying hens. This condition compromises bird welfare, productivity, and economic sustainability within commercial farming systems. This narrative review provides a comprehensive overview of the underlying mechanisms through which hepatic lipid accumulation, metabolic dysfunctions, hormonal imbalances, genetic susceptibilities, and environmental stress contribute to the development of NAFLD. The multifactorial nature of NAFLD is explored through a critical assessment of the literature, highlighting the influence of diet composition, management practices, and physiological demands associated with intensive egg production. Emphasis is placed on recent advancements in nutritional modulation, selective breeding, and housing improvements aimed at prevention and mitigation of NAFLD. Furthermore, the review identifies key research gaps, including limited understanding of epigenetic influences and the long-term efficacy of intervention strategies. An integrative framework is advocated, synergizing genetics, nutrition, and environmental optimization to effectively address the complexity of NAFLD in poultry and supports the development of resilient production systems. The insights presented aims to inform both future research and practical applications for enhancing poultry health and performance.

Dietary fiber contributes to improving intestinal morphology, barrier integrity, and microbial balance, thereby enhancing nutrient utilization and growth performance in animals. This study evaluated the effects of supplementing lignocellulose on intestinal function and growth performance in meat ducks. A total of 180 one-day-old Cherry Valley ducks were randomly assigned to the control group (CON), lignocellulose group 1 (LC1), and lignocellulose group 2 (LC2) (6 replicates each group, 10 ducks each replicate). Ducks in the CON group were fed a basal diet; the LC1 group received the basal diet supplemented with 0.6% lignocellulose from days 1 to 42, while the LC2 group received the basal diet supplemented with 0.3% lignocellulose from days 1 to 21 and 0.6% from days 22 to 42. Lignocellulose supplementation increased average daily gain in the LC1 group (P< 0.05), and improved feed conversion ratio in the LC2 group before day 28 (P< 0.05). Additionally, lignocellulose increased intestinal length (P< 0.05) and weight (P< 0.05), and improved the intestinal structure (P< 0.05) and antioxidant capacity (P< 0.05). However, the expression of genes associated with tight junctions, immunity, and inflammation was not significantly affected. Overall, dietary lignocellulose promotes growth in meat ducks by improving intestinal morphology and antioxidant capacity without affecting the expression of genes involved in intestinal tight junction and immunity or inflammation. The magnitude of benefits depends on the supplementation level, duration, and the age of birds.

Our study presents the assembly of a high-quality Taihu goose genome at the Telomere-to-Telomere (T2T) level. By employing advanced sequencing technologies, including Pacific Biosciences HiFi reads, Oxford Nanopore long reads, Illumina short reads, and chromatin conformation capture (Hi-C), we achieved an exceptional assembly. The T2T assembly encompasses a total length of 1,197,991,206 bp, with contigs N50 reaching 33,928,929 bp and scaffold N50 attaining 81,007,908 bp. It consists of 73 scaffolds, including 38 autosomes and one pair of Z/W sex chromosomes. Importantly, 33 autosomes were assembled without any gap, resulting in a contiguous representation. Furthermore, gene annotation efforts identified 34,898 genes, including 436,162 RNA transcripts, encompassing 806,158 exons, 743,910 introns, 651,148 coding sequences (CDS), and 135,622 untranslated regions (UTR). The T2T-level chromosome-scale goose genome assembly provides a vital foundation for future genetic improvement and understanding the genetic mechanisms underlying important traits in geese.