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| (a) Clinical scores for chicken livers were divided into six levels representing different degrees of FLS. (b) Chicken livers were stained with HE, viewed under a microscope (100×, 400×, and 600×), and assigned pathological scores representing the degree of FLS. The categorization scheme is shown in Table 5.
Source publication
This study investigated the molecular mechanism underlying the effect of dietary genistein (GEN) on fatty liver syndrome (FLS) in laying hens. Hens in the control group (CG) were fed a high-energy and low-choline (HELC) diet to establish the FLS model. The livers of the FLS hens were friable and swollen from hemorrhage. Hepatic steatosis and inflam...
Contexts in source publication
Context 1
... is shown in Figure 2a, we classified the fatty liver severity into six levels according to the hepatic clinical scores. We defined levels 3 to 6 as the FLS. ...
Context 2
... hepatic clinical scores of the LGE and HGE group were significantly lower than that of the CON group (P < 0.05), indicating the favorable, anti-FLS effect of GEN. In terms of histological changes, we observed hepatocyte tumefaction and focal necrosis in the CON group (Figure 2b). The hepatocytes of the CON group contained fat vacuoles of various sizes, which pushed the nuclei aside. ...
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Citations
... For decades, chickens have been used as a model to study obesity, adipose biology, and insulin resistance (Mellouk et al. 2018). Our findings demonstrate similar metabolic syndromes as seen in humans during NAFLD such as obesity, hyperlipidemia, hypercholesterolemia, and hypertriglyceridemia. Similar results were described in the hens that were fed a highenergy and low choline diet (Lv et al. 2018). However, the study used 80-week-old JINGFEN 1 laying hen compared to 3-week-old white leghorn chicken irrespective of sex used in our study. ...
Nonalcoholic fatty liver disease (NAFLD), which shows similar symptoms as fatty liver hemorrhage syndrome (FLHS) in chickens, is the most common cause of chronic liver disease and cancer in humans. NAFLD patients and FLHS in chickens have demonstrated severe liver disorders when infected by emerging strains of human hepatitis E virus (HEV) and avian HEV, respectively. We sought to develop a fatty liver disease chicken model by altering the diet of 3-week-old white leghorn chickens. The high cholesterol, and low choline (HCLC) diet included 7.6% fat with additional 2% cholesterol and 800 mg/kg choline in comparison to 5.3% fat, and 1,300 mg/kg choline in the regular diet. Our diet induced fatty liver avian model successfully recapitulates the clinical features seen during NAFLD in humans and FLHS in chickens, including hyperlipidemia and hepatic steatosis, as indicated by significantly higher serum triglycerides, serum cholesterol, liver triglycerides, cholesterol, and fatty acids. By developing this chicken model, we expect to provide a platform to explore the role of lipids in the liver pathology linked with viral infections and contribute to the development of prophylactic interventions.
... Similar to our findings, Zengpeng and colleagues demonstrated that dietary genistein supplementation resulted in the upregulation of gene transcription associated with fatty acid beta-oxidation, including PPARα, PPARδ, ACOT8, ACAD8, and ACADs in the liver of laying hens induced fatty liver. Additionally, this treatment led to a reduction in the expression of PPARγ and AFABP in abdominal fat [15]. STAT1 is another key mediator of chronic inflammatory response and is activated in chronic liver diseases [51]. ...
... An in vitro study by Jantaratnotai et al. found that treatment with genistein (1 µM) significantly inhibited the upregulation of iNOS, IRF-1, and p-STAT1 protein expression induced via LPS-activated microglia [52]. Moreover, dietary genistein had the potential to directly alleviate the inflammatory response by modulating the expression of inflammatory factors such as NF-кB, IL-8, IL-1β, and IFN-γ through the involvement of PPARδ and T-cell factor 3 (TCF3) in laying hens induced fatty liver [15]. Therefore, the inhibition of STAT1 activation by IFN-γ receptor may be responsible for the immune-modulatory effects of genistein in NASH; however, the precise interactions between STAT1 and IFN-γ required further investigation. ...
Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that is characterized by hepatic inflammation and steatosis. Currently, limited data exist regarding the risk of NASH in transgender women and the treatment options for this particular population. The use of testosterone supplementation is unfavorable for transgender women, and estrogen supplementation is linked to an increased risk of breast cancer; thus, an isoflavone derivative compound known as “genistein” could serve as a viable substitute for a hormone supplement in this context. The purpose of this study was to investigate the treatment effects and mechanisms of actions of genistein and sex hormones in orchidectomized (ORX) rats with nonalcoholic steatohepatitis induced via a high-fat high-fructose diet (HFHF) model. Male Sprague-Dawley rats (n = 42) were randomly assigned into seven groups; control, ORX + standard diet, HFHF, ORX + HFHF, ORX + HFHF diet + testosterone (50 mg/kg body weight (BW) once weekly), ORX + HFHF diet + estradiol (1.6 mg/kg BW daily), and ORX + HFHF diet + genistein (16 mg/kg BW daily). The duration of the study was 6 weeks. Some parts of liver tissue were used for histological examination by H&E staining. The determination of fat accumulation was performed using Oil Red O staining. SREBP1c and FAS gene expression were quantified using real-time PCR technique. The levels of all types of peroxisome proliferator-activated receptors (PPARs; α, δ, γ), proteins, and signal transducer and activator of transcription 1 (STAT1) signaling pathway were determined by both immunoblotting and immunohistochemistry. Rats in the ORX + HFHF group had the highest degree of hepatic steatosis, lobular inflammation, and hepatocyte ballooning, and showed higher levels of genes related to de novo lipogenesis, including SREBP1c and FAS. The expression of PPARγ and STAT1 were upregulated, while the expression of PPARα and PPARδ were downregulated in the ORX + HFHF group. Testosterone, estradiol and genistein treatments improved NASH histopathology together with the reversal of all types of PPAR protein expressions. Interestingly, genistein decreased the levels of STAT1 protein expression more than those of testosterone and estradiol treatment. Genistein and sex hormone treatment could ameliorate NASH through the upregulation of PPARα, and PPARδ, and the suppression of PPARγ and STAT1 expression.
... The histological changes observed in the livers of these hens provide evidence for anatomical pathological features. The hepatocyte exhibited similarities to those previously described for NAFLD [50]. Administration of PM or succinate can induce alterations in the pathological changes, thereby indicating a potential alleviation of the TGs accumulation in the liver of laying hens. ...
... Mitochondrial dysfunction can lead to electron leakage at respiratory complexes, resulting in the excess accumulation of ROS. And excessive ROS can disrupt the balance between oxidation and antioxidation, inducing lipid oxidation, DNA damage and ultimately resulting in poor production performance in aged hens [50,58]. MDA is a significant oxidation product derived from peroxidized polyunsaturated fatty acids and serves as a crucial marker for assessing lipid peroxidation [59]. ...
Background
This work aimed to investigate the potential benefits of administering Prevotella and its primary metabolite succinate on performance, hepatic lipid accumulation and gut microbiota in laying hens.
Results
One hundred and fifty 58-week-old Hyline Brown laying hens, with laying rate below 80% and plasma triglyceride (TG) exceeding 5 mmol/L, were used in this study. The hens were randomly allocated into 5 groups and subjected to one of the following treatments: fed with a basal diet (negative control, NC), oral gavage of 3 mL/hen saline every other day (positive control, PC), gavage of 3 mL/hen Prevotella melaninogenica (10 ⁷ CFU/mL, PM) or 3 mL/hen Prevotella copri (10 ⁷ CFU/mL, P. copri ) every other day, and basal diet supplemented with 0.25% sodium succinate (Succinate). The results showed that PM and P. copri treatments significantly improved laying rate compared to the PC ( P < 0.05). The amount of lipid droplet was notably decreased by PM, P. copri , and Succinate treatments at week 4 and decreased by P. copri at week 8 ( P < 0.05). Correspondingly, the plasma TG level in Succinate group was lower than that of PC ( P < 0.05). Hepatic TG content, however, was not significantly influenced at week 4 and 8 ( P > 0.05). PM treatment increased ( P < 0.05) the mRNA levels of genes PGC-1β and APB-5B at week 4, and ACC and CPT-1 at week 8. The results indicated enhanced antioxidant activities at week 8, as evidenced by reduced hepatic malondialdehyde (MDA) level and improved antioxidant enzymes activities in PM and Succinate groups ( P < 0.05). Supplementing with Prevotella or succinate can alter the cecal microbiota. Specifically, the abundance of Prevotella in the Succinate group was significantly higher than that in the other 4 groups at the family and genus levels ( P < 0.05).
Conclusions
Oral intake of Prevotella and dietary supplementation of succinate can ameliorate lipid metabolism of laying hens. The beneficial effect of Prevotella is consistent across different species. The finding highlights that succinate, the primary metabolite of Prevotella , represents a more feasible feed additive for alleviating fatty liver in laying hens.
... In addition, further analysis conducted through HE staining indicated the occurrence of various pathological injuries resulting from the HELP diet, including hepatocyte steatosis, lipid droplet accumulation, and altered hepatocyte shape. These results performed in our research were found to be in line with previous literature [36,37], which has demonstrated that the HELP diet can trigger the development of FLHS in laying hens. However, we noticed that the typical symptoms of FLHS were ameliorated when CSB was introduced into the diet. ...
Background:
Fatty liver hemorrhagic syndrome (FLHS), a fatty liver disease in laying hens, poses a grave threat to the layer industry, stemming from its ability to trigger an alarming plummet in egg production and usher in acute mortality among laying hens. Increasing evidence suggests that the onset and progression of fatty liver was closely related to mitochondria dysfunction. Sodium butyrate was demonstrated to modulate hepatic lipid metabolism, alleviate oxidative stress and improve mitochondrial dysfunction in vitro and mice models. Nevertheless, there is limited existing research on coated sodium butyrate (CSB) to prevent FLHS in laying hens, and whether and how CSB exerts the anti-FLHS effect still needs to be explored. In this experiment, the FLHS model was induced by administering a high-energy low-protein (HELP) diet in laying hens. The objective was to investigate the effects of CSB on alleviating FLHS with a focus on the role of CSB in modulating mitochondrial function.
Methods:
A total of 288 healthy 28-week-old Huafeng laying hens were arbitrarily allocated into 4 groups with 6 replicates each, namely, the CON group (normal diet), HELP group (HELP diet), CH500 group (500 mg/kg CSB added to HELP diet) and CH750 group (750 mg/kg CSB added to HELP diet). The duration of the trial encompassed a period of 10 weeks.
Results:
The result revealed that CSB ameliorated the HELP-induced FLHS by improving hepatic steatosis and pathological damage, reducing the gene levels of fatty acid synthesis, and promoting the mRNA levels of key enzymes of fatty acid catabolism. CSB reduced oxidative stress induced by the HELP diet, upregulated the activity of GSH-Px and SOD, and decreased the content of MDA and ROS. CSB also mitigated the HELP diet-induced inflammatory response by blocking TNF-α, IL-1β, and F4/80. In addition, dietary CSB supplementation attenuated HELP-induced activation of the mitochondrial unfolded protein response (UPRmt), mitochondrial damage, and decline of ATPase activity. HELP diet decreased the autophagosome formation, and downregulated LC3B but upregulated p62 protein expression, which CSB administration reversed. CSB reduced HELP-induced apoptosis, as indicated by decreases in the Bax/Bcl-2, Caspase-9, Caspase-3, and Cyt C expression levels.
Conclusions:
Dietary CSB could ameliorate HELP diet-induced hepatic dysfunction via modulating mitochondrial dynamics, autophagy, and apoptosis in laying hens. Consequently, CSB, as a feed additive, exhibited the capacity to prevent FLHS by modulating autophagy and lipid metabolism.
... Existing studies have confirmed that ACOT8 catalyzes the hydrolysis of all fatty acyl-CoA [46], and that its activity is regulated by PPARα and CoASH levels [43,44]. Based on the available research results and the results of this trial, we hypothesized that upregulation of ACOT8 suppressed fatty acid synthesis and enhanced β oxidation, thereby inhibiting fat synthesis [47]. ...
Subcutaneous fat deposition is an important index with which to evaluate meat-producing ducks, and affects their meat quality and feed conversion rate. Studying the differentially expressed genes in subcutaneous fat will help to comprehensively understand the potential mechanisms regulating fat deposition in ducks. In this study, 72 Nankou 1 Pekin Ducks and 72 Jingdian Pekin Ducks (half male and half female) at 42 days of age were selected for slaughter performance and transcriptome analysis. The results showed that the breast-muscle yield of Nankou 1 ducks was significantly higher than that of Jingdian ducks, but that the abdominal fat yield and subcutaneous fat yield were higher than that of Jingdian ducks. Thousands of DEGs, including many important genes involved in fat metabolism regulation, were detected by transcriptome. KEGG enrichment analysis showed that the DEGs were significantly enriched on pathways such as regulation of lipolysis in adipocytes, primary bile acid biosynthesis, and biosynthesis of unsaturated fatty acids. SCD, FGF7, LTBP1, PNPLA3, ADCY2, and ACOT8 were selected as candidate genes for regulating subcutaneous fat deposition. The results indicated that Nankou 1 had superior fat deposition ability compared to Jingdian ducks, and that the candidate genes regulated fat deposition by regulating fat synthesis and decomposition.
... The AMPK functions as an energy sensor, playing an important role in autophagy, metabolic homeostasis, and lipid deposition (Yao et al., 2022a). The PPARa is a regulator of lipid metabolism via mitochondrial b-oxidation and microsomal v-oxidation (Lv et al., 2018). There is a positive correlation between ucOCN and ADPN (El Amrousy and El-Afify, 2020). ...
... The addition of ucOCN significantly alleviated hepatocyte lipid accumulation via the AMPK signaling pathway in oleic acid/palmitic acid treated HepG2 cells . Furthermore, PPARa and ucOCN can regulate lipid and lipoprotein metabolism and glucose hemostasis (Lv et al., 2018;Tacey et al., 2021). However, there need further study to investigate whether lipophagy play an important role in cellular mechanisms underlying ucOCN effects on the lipid metabolism. ...
Fatty liver hemorrhage syndrome (FLHS) is the leading cause of noninfectious mortality in caged layers worldwide. Osteocalcin (OCN) is a protein secreted by osteoblasts, and its undercarboxylated form (ucOCN) acts as a multifunctional hormone that protects laying hens from FLHS. Lipophagy is a form of selective autophagy that breaks down lipid droplets (LDs) through lysosomes, and defective lipophagy is associated with FLHS. The aim of this study was to investigate the effects of ucOCN on the lipophagy of chicken embryonic hepatocytes and associated the function of the adiponectin (ADPN) signaling pathway. In this study, chicken embryonic hepatocytes were divided into 5 groups: control (CONT), fat emulsion (FE, 10% FE, v/v), FE with ucOCN at 1 ng/mL (FE-LOCN), 3 ng/mL (FE-MOCN), and 9 ng/mL (FE-HOCN). In addition, 4 μM AdipoRon, an adiponectin receptor agonist, was used to investigate the function of ADPN. The results showed that compared with CONT group, FE promoted the levels of phosphorylation of mammalian target of rapamycin (p-mTOR) (P < 0.05) and decreased the mRNA expression of ADNP receptors (AdipoR1 and AdipoR2). Compared with FE group, 3 and 9 ng/mL ucOCN inhibited the levels of autophagy adaptor p62 and p-mTOR (P < 0.05), increased the ratios of LC3-II/LC3-I (P < 0.05) and phosphorylated adenosine 5′-monophosphate-activated protein kinase (p-AMPK)/AMPK (P < 0.05), as well as the levels of peroxisome proliferator-activated receptor α (PPAR-α) and ADPN (P < 0.05). In addition, ucOCN at the tested concentrations increased the colocalization of LC3 and LDs in fatty hepatocytes. Administrated 4 μM AdipoRon activated AdipoR1 and AidpoR2 mRNA expression (P < 0.05), decreased the concentrations of triglyceride (P < 0.05), without effects on cell viability (P > 0.05). AdipoRon also increased the LC3-II/LC3-I ratio (P < 0.05) and the levels of p-AMPK/AMPK and PPAR-α (P < 0.05). In conclusion, the results reveal that ucOCN regulates lipid metabolism by activating lipophagy via the ADPN-AMPK/PPARα-mTOR signaling pathway in chicken embryonic hepatocytes. The results may provide new insights for controlling FLHS in laying hens.
... Aging can also affect the health status of laying hens, and fatty liver hemorrhagic syndrome (FLHS) is one of the most common metabolic diseases in laying hens during the late laying period. FLHS can significantly decrease egg production and induce sudden death, resulting in major economic losses for the poultry industry (Lv et al., 2018). The pathogenesis of FLHS remains unclear. ...
... One of the most prevalent metabolic disorders in laying hens is FLHS, characterized by an abnormal accumulation of fat in the liver which can reduce egg production and, in the most severe cases, result in the sudden death of the birds (Lv et al., 2018). Due to their relatively simple lymphatic systems, chickens are susceptible to accumulating fat in their liver because dietary fat flows directly into the portal vein (Davis et al., 2016). ...
In this study, we evaluated the enrichment efficiency of lutein in eggs and its function in preventing fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Five groups of laying hens (65 weeks old) were fed basal diets supplemented with 0, 30, 60, 90, or 120 mg/kg of lutein. The supplementation period lasted 12 weeks followed by 2 weeks of lutein depletion in feed. The results revealed that lutein efficiently enriched the egg yolks and improved their color with a significant increase in relative redness (P < 0.001). Lutein accumulation increased in the egg yolk until day 10, then depletion reached a minimum level after 14 days. Overall, zeaxanthin content in all the groups was similar throughout the experimental period. However, triglycerides and total cholesterol were significantly decreased in the liver (P < 0.05) but not significantly different in the serum (P > 0.05). In the serum, the lipid metabolism enzyme acetyl-CoA synthetase was significantly reduced (P < 0.05), whereas dipeptidyl-peptidase 4 was not significantly different (P > 0.05), and there was no statistical difference of either enzyme in the liver (P > 0.05). Regarding oxidation and inflammation-related indexes, malondialdehyde, tumor necrosis factors alpha, interleukin-6, and interleukin-1 beta were decreased, whereas superoxide dismutase and total antioxidant capacity increased in the liver (P < 0.001). The function of lutein for the same indexes in serum was limited. It was concluded that lutein efficiently enriched the egg yolk of old laying hens to improve their color and reached the highest level on day 10 without being subject to a significant conversion into zeaxanthin. At the same time, lutein prevented liver steatosis in aged laying hens by exerting strong antioxidant and anti-inflammatory functions, but also through the modulation of lipid metabolism, which may contribute to reducing the incidence of FLHS in poultry.
... Notably, treatment with GEN effectively suppressed the chronic HS-challenged enhancements in the gene expression of lipid synthesisrelated factors in the livers of broilers. Numerous studies have previously demonstrated that GEN possesses the ability to inhibit fatty acid synthesis in poultry and rodents (Lv et al., 2018b;Pummoung et al., 2020). Furthermore, our recent investigations have provided evidence of the ability of GEN to inhibit fatty acid synthesis both in primary chicken hepatocytes and broilers (Jiang et al., , 2023. ...
The objective of this study was to investigate the preventive effects and mechanisms of genistein (GEN) on production performance and metabolic disorders in broilers under chronic heat stress (HS). A total of 120 male 3-wk-old Ross broilers were randomly assigned to 5 groups: a thermoneutral zone (TN) group maintained at normal temperature (21°C ± 1°C daily), an HS group subjected to cyclic high temperature (32°C ± 1°C for 8 h daily), and 3 groups exposed to HS with varying doses of GEN (50, 100, or 150 mg/kg diet). The experimental period lasted for 3 wk. Here, HS led to a decline in growth performance parameters and hormone secretion disorders (P < 0.05), which were improved by 100 and 150 mg/kg GEN treatment (P < 0.05). Moreover, the HS-induced increases in the liver index (P < 0.01) and abdominal fat rate (P < 0.05) were attenuated by 150 mg/kg GEN (P < 0.05). The HS-induced excessive lipid accumulation in the liver and serum (P < 0.01) was ameliorated after 100 and 150 mg/kg GEN treatment (P < 0.05). Furthermore, the HS-induced decreases in lipolysis-related mRNA levels and increases in lipid synthesis-related mRNA levels in the liver (P < 0.01) were effectively blunted after 100 and 150 mg/kg GEN treatment (P < 0.05). Importantly, the HS-stimulated hepatic mitochondrial energetic dysfunction and decreases in the mRNA or protein levels of peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α), nuclear respiratory factor 1, and mitochondrial transcription factor A in the liver were ameliorated by 150 mg/kg GEN (P < 0.05). Moreover, 50 to 150 mg/kg GEN treatment resulted in a significant increase in the mRNA or protein levels of G protein-coupled estrogen receptor (GPR30), AMP-activated protein kinase (AMPK) α1, phosphorylated AMPKα, and phosphorylated acetyl-CoA carboxylase α. Collectively, GEN alleviated metabolic disorders and hepatic mitochondrial energetic dysfunction under HS, possibly through the activation of GPR30-AMPM-PGC-1α pathways. These data provide a sufficient basis for GEN as an additive to alleviate HS in broilers.
... In the late stage of production, laying hens often exhibit perturbed lipid metabolism characterized by hepatic lipid deposition and abdominal fat accumulation [62]. This dysregulation of lipid metabolism has the potential to profoundly impact the production performance of laying hens [63]. The evaluation of blood lipid levels utilized TG, T-CHO, FFA, LDL, and Gly as markers. ...
Probiotics gained significant attention for their potential to improve gut health and enhance productivity in animals, including poultry. This comprehensive study focused on the genetic analysis of Lactiplantibacillus plantarum 18 (LP18) to understand its survival and colonization characteristics in the gastrointestinal tract. LP18 was supplemented in the late-stage diet of laying hens to investigate its impact on growth performance, egg quality, and lipid metabolism. The complete genome sequence of LP18 was determined, consisting of 3,275,044 base pairs with a GC content of 44.42% and two circular plasmids. Genomic analysis revealed genes associated with adaptability, adhesion, and gastrointestinal safety. LP18 supplementation significantly improved the daily laying rate (p < 0.05) during the late-production phase and showed noteworthy advancements in egg quality, including egg shape index (p < 0.05), egg albumen height (p < 0.01), Haugh unit (p < 0.01), and eggshell strength (p < 0.05), with notable improvements in eggshell ultrastructure. Additionally, LP18 supplementation resulted in a significant reduction in serum lipid content, including LDL (p < 0.01), FFA (p < 0.05), and Gly (p < 0.05). These findings provide valuable insights into the genomic characteristics of LP18 and the genes that support its survival and colonization in the gastrointestinal tract. Importantly, this study highlights the potential of LP18 as a probiotic candidate to enhance productivity, optimize egg quality, and modulate lipid metabolism in poultry production.
... The laying performance of local breeds of chickens differs considerably from that of commercial laying hens and remains so during the late laying period [22]. The liver is the major organ of energy metabolism and fatty acid metabolism [21], and yolk deposition in the follicle depends on the transport of lipids and proteins from the liver to the ovary [23]. In this study, the proteomic and metabolomic profiles were compared between the liver and ovary of 55-week-old Guangyuan gray chickens and Hy-Line gray chickens. ...
... Morphological and histological studies showed that the livers of Group H were yellowish in color, with more loosely arranged liver cells, and were richer in lipid droplets than those of Group G under the same feeding conditions. The altered morphology of liver cells in Group H may be attributed to the long-term absorption of large amounts of nutrients, such as TC and TG, by the liver in order to maintain a high egg production [23]. Eventually, the fat absorbed by the liver exceeds the transport capacity of the apolipoproteins, leading to fatty liver syndrome (FLS) [24]. ...
The liver and ovary perform a vital role in egg production in hens. In the later laying period, the egg-laying capacity of female hens, particularly that of local breeds, declines significantly. Hence, it is essential to study the features and conditions of the ovary and liver during this period. In this research, we characterized the proteins and metabolites in the liver and ovary of 55-week-old Guangyuan gray chickens (Group G) and Hy-Line gray chickens (Group H) by using liquid chromatography chip/electrospray ionization quadruple time-of-flight/mass spectroscopy (LC-MS/MS). In total, 139 differentially expressed proteins (DEPs) and 186 differential metabolites (DMs) were identified in the liver, and 139 DEPs and 36 DMs were identified in the ovary. The upregulated DEPs and DMs in both the liver and ovary of Group G were primarily enriched in pathways involved in amino acid and carbohydrate metabolism. This suggests that energy metabolism was highly active in the Guangyuan gray chickens. In contrast, the upregulated DEPs and DMs in Group H were mainly enriched in pathways associated with lipid metabolism, which may explain the higher egg production and the higher fatty liver rate in Hy-Line gray hens in the later laying period. Additionally, it was found that the unique protein s-(hydroxymethyl) glutathione dehydrogenase (ADH4) in Group G was implicated in functions such as fatty acid degradation, glycolysis, and pyruvate metabolism, whereas the unique proteins, steroid sulfatase (STS), glucosylceramidase (LOC107050229), and phospholipase A2 Group XV (PLA2G15), in Group H were involved in the metabolism of steroid hormones and glycerol phosphate. In conclusion, variations in how carbohydrates, lipids, and amino acids are processed in the liver and ovary of local breeds of chicken and commercial hens towards the end of their laying period could explain the disparities in their egg production abilities.
