Prevalence and Pathology of Fatty Liver Hemorrhagic Syndrome in Kadaknath under Different Rearing Systems

Total flavonoids from Abrus cantoniensis alleviate fatty liver hemorrhagic syndrome in laying hens by regulating inflammation, oxidative stress, and cecal metabolites and microbiota.

Quantitative lipidomics reveals the changes of lipids and antioxidant capacity in egg yolk from laying hens with fatty liver hemorrhagic syndrome

Fatty liver haemorrhagic syndrome (FLHS) is a widespread metabolic disease in laying hens that causes a decrease in egg production and even death. Insulin resistance is a major contributor to the pathogenesis of nonalcoholic fatty liver disease. However, the relationship between FLHS and the insulin resistance mechanisms underlying FLHS is not well elucidated. Therefore, we established an FLHS model induced by feeding a high-energy low-protein diet. In the current study, we found that the fasting glucose and insulin concentrations were elevated in the FLHS group compared with the control group during the experimental period. The results of the oral glucose tolerance test (OGTT) and insulin sensitivity test (IST) showed a high level of insulin resistance in the FLHS model. InsR, 4EBP-1, Glut-1 and Glut-3 mRNA expression were decreased, and TOR, S6K1, and FOXO1 were elevated (P < 0.05). Metabolomic analysis with GC/MS identified 46 differentially expressed metabolites between these two groups, and of these, 14 kinds of metabolism molecules and 32 kinds of small metabolism molecules were decreased (P < 0.05). Further investigation showed that glucose, lipid and amino acid metabolism blocks in the progression of FLHS by GO functional and pathway analysis. Overall, these results suggest that insulin resistance participated in FLHS; comprehensively, metabolites participated in the dysregulated biological process.

Untargeted and targeted metabolomics profiling reveals the underlying pathogenesis and abnormal arachidonic acid metabolism in laying hens with fatty liver hemorrhagic syndrome

Glyphosate below no-observed-adverse-effect level exacerbates fatty liver hemorrhagic syndrome in laying hens

Quantitative lipidomics reveals lipid perturbation in the liver of fatty liver hemorrhagic syndrome in laying hens

Fatty liver hemorrhagic syndrome (FLHS) is a common metabolic disease in birds. FLHS have highly incidence rate in cage system. The syndrome can be characterized by abnormal lipid accumulation in liver which trigger inflammation and hemorrhage syndrome. Moreover, FLHS decrease egg production severely and have huge impact to the poultry industry. Additionally, FLHS is similar diagnosis to non‐alcoholic fatty liver disease (NAFLD). NAFLD is a spectrum of liver disorders and characterized by excessive hepatic fat accumulation. Ganoderma lucidum ( G. lucidum ) is a medicinal mushroom. G. lucidum is rich in bioactive components comprises and has hepatoprotective activity. Dipeptidyl‐peptidase 4 (DPP4) is a type II transmembrane protein and strongly associated with FLHS and NAFLD. The objective of this study was to determine the effects of feeding diets containing different ratio of G. lucidum on FLHS and the association of plasma DPP4 in hens and to use LMH cell to study the role of DPP4 in FLHS. Thirty 7‐week‐old, ISA hens were allotted to 5 treatments with 6 hens per replicate and fed high cholesterol low choline (CLC), CLC + 0.25% G. lucidum , CLC + 0.5% G. lucidum , CLC + 0.75% G. lucidum , and CLC + 1% G. lucidum , respectively, for six weeks. Body weight and plasma were recorded every three week. At the end of experiment, livers were photographed, excised, weighed, and scored for liver hemorrhages. The results showed that CLC + 1% G. lucidum body weight was significantly higher than CLC + 0.25% G. lucidum and treatment of G. lucidum decreased the level of triglyceride in the plasma. Oleic acid induced DPP4 mRNA expression in LMH cells, suggesting that there is an association between lipid and DPP4 expression in the liver cell. In conclusion, G. lucidum could be a dietary additive or medicine for reducing fatty liver in laying hen s.

Cidea and Cidec are two members of Cell death-inducing DNA fragmentation factor-alpha-like effector family proteins, which could be involved in lipid or fat metabolism. To better understand the roles of Cidea and Cidec in fatty liver hemorrhagic syndrome (FLHS), 150 healthy 155-day-old Hyline Brown laying hens were randomly divided into control group (fed with basic diet) and experimental group (fed with high-energy low-protein [HELP] diet). Analysis of the liver by tissue sectioning and hematoxylin and eosin staining showed that the HELP diet induced micro-vesicular steatosis in laying hens. Subsequently, based on the liver color scores and the range of lipid accumulation observed in histological examination, we classified livers with <50% vacuolization as mild FLHS and >50% as severe FLHS. The results showed that the levels of Cidea and Cidec mRNA expression were markedly elevated in the liver and adipose tissues with FLHS and the levels of Cidea and Cidec mRNA expression in the liver with severe FLHS were significantly higher than that in the liver with mild FLHS. Thus, the present study revealed that the Cidea and Cidec genes may be involved in pathways of FLHS formation.

1. A total of 90 healthy Hyline brown laying hens (44 weeks old) were randomly assigned into three groups, a group of hens with fatty liver haemorrhagic syndrome (FLHS) fed with high-energy low-protein diet (HELPD), which exacerbates the syndrome, and the other two groups fed with HELPD containing 400 and 800 mg/kg PSP, respectively, to investigate the therapeutic effects and underlying mechanisms of Polygonatum sibiricum polysaccharides (PSP) on FLHS. 2. Dietary PSP supplementation significantly elevated laying rate of FLHS hens. The FLHS hens fed with PSP displayed significant decrease in ALT, AST, TG, TC and LDL-C, while the increase in ALB, TP and HDL-C compared with FLHS hens. 3. Hens receiving PSP had significantly reduced levels of MDA but increased activity of T-AOC, SOD, CAT and GSH-Px in both the serum and liver of hens with FLHS. It inhibited inflammatory response in FLHS hens, as evidenced by reduced levels and expression of IL-1β, TNF-α and IL-6, but elevated levels and expression of IL-10 in the serum and liver. 4. Transcriptome analysis confirmed that PSP improved FLHS in laying hens through regulating lipid metabolism (such as PPAR signalling pathway, fatty acid metabolism and fatty acid biosynthesis), redox balance (including FoxO signalling pathway and peroxisome) and inflammation (e.g. adipocytokine signalling pathway and cytokine–cytokine receptor interaction). 5. This study indicated that dietary PSP supplementation is a practical strategy to prevent and treat FLHS through improving lipid deposition, oxidative stress and inflammation in laying hens.

Background：Fatty liver hemorrhagic syndrome (FLHS) in the modern poultry industry is primarily caused by nutrition. Despite encouraging progress on FLHS, the mechanism through which nutrition influences susceptibility to FLHS is still lacking in terms of epigenetics. Results: In this study, we analyzed the genome-wide patterns of trimethylated lysine residue 27 of histone H3 (H3K27me3) enrichment by chromatin immunoprecipitation-sequencing (ChIP-seq), and examined its association with transcriptomes in healthy and FLHS hens. The study results indicated that H3K27me3 levels were increased in the FLHS hens on a genome-wide scale. Additionally, H3K27me3 was found to occupy the entire gene and the distant intergenic region, which may function as silencer-like regulatory elements. The analysis of transcription factor (TF) motifs in hypermethylated peaks has demonstrated that 23 TFs are involved in the regulation of liver metabolism and development. Transcriptomic analysis indicated that differential expressed genes (DEGs) were enriched in fatty acid metabolism, amino acid, and carbohydrate metabolism. The hub gene identified from PPI network is fatty acid desaturase-like 1 (FADS1). Combined ChIP-seq and transcriptome analysis revealed that the increased H3K27me3 and down-regulated genes have significant enrichment in the ECM-receptor interaction, tight junction, cell adhesion molecules, adherens junction, and TGF-beta signaling pathways. Conclusions: Overall, the trimethylation modification of H3K27 has been shown to have significant regulatory function in FLHS, mediating the expression of crucial genes associated with the ECM-receptor interaction pathway. This highlights the epigenetic mechanisms of H3K27me3 and provides insights into exploring core regulatory targets and nutritional regulation strategies in FLHS.

Dioscin improves fatty liver hemorrhagic syndrome by promoting ERα-AMPK mediated mitophagy in laying hens

Background: Fatty liver hemorrhagic syndrome (FLHS) is a metabolic condition occurring worldwide in caged layers and causes significant losses to the egg industry.Aims: to determine the main pathological, metabolic and performance changes in layers affected by fatty liver haemorrhagic syndrome.Methods: The present study includes a (300) laying hens at the age fifty-three weeks from six farms suffering from the fatty liver hemorrhagic syndrome. changes in body weight, feed intake, feed conversion rate was determined. blood samples were taken from brachial vein to determine albumin, globulin, total protein, albumin/ globulin, blood urea nitrogen, cholesterol, calcium, glucose, phosphorus. alt, alp, creatinine and creatine kinase. Full postmortem examination was performed and histopathological examination for liver sections stained with hematoxylin and eosin.Results: Positive significant correlation was reported between body weight gain and feed intake (R= 0.703, P value = 0.000). Positive significant correlation was reported between body weight gain and feed conversion rate (R= 0.850, P value = 0.000). Positive significant correlation was reported between body weight gain and liver lesion score (R= 0.524, P value = 0.000). Significant difference was reported between hens with FLHS and normal hens regarding the values of albumin (P value = 0.000), albumin/ globulin (P value = 0.0018), globulin (P value = 0.009533), total protein (P value = 0.0000). Significant difference was reported between hens with FLHS and normal hens regarding the values of alkaline phosphatase (P value = 0.0000), No significant difference was reported between hens with FLHS and normal hens regarding the values of ALT (P value = 0.57339). Significant difference was reported between hens with FLHS and normal hens regarding the values of creatinine (P value = 0.00003421), creatine kinase (P value = 0.0000). Significant difference was reported between hens with FLHS and normal hens regarding the values of blood urea nitrogen (P value = 0.0015), cholesterol (P value = 0.00000), calcium (P value = 0.0000), phosphorus (P value = 0.000034), glucose (P value = 0.0000). Necropsy findings reveals abdomen filled with large blood spots with hepatomegaly and fat deposition. Liver usually friable and presented with yellow, pale or putty colors. Histopathological necrosis for hepatic cords with moderate dilation and congestion of sinusoidal together with wide hemorrhages.Conclusions: FLHS induced mainly with consumption of high energy diet causing serious negative effects on liver function as well as most vital metabolic biomarkers in laying hens

The feeding of high-energy and low-protein diets often induces fatty liver hemorrhagic syndrome (FLHS) in laying hens. However, the mechanism of hepatic fat accumulation in hens with FLHS remains uncertain. In this research, a comprehensive hepatic proteome and acetyl-proteome analysis was performed in both normal and FLHS-affected hens. The results indicated that the upregulated proteins were primarily associated with fat digestion and absorption, the biosynthesis of unsaturated fatty acids, and glycerophospholipid metabolism, while the downregulated proteins were mainly related to bile secretion and amino acid metabolism. Furthermore, the significant acetylated proteins were largely involved in ribosome and fatty acid degradation, and the PPAR signaling pathway, while the significant deacetylated proteins were related to valine, leucine, and isoleucine degradation in laying hens with FLHS. Overall, these results demonstrate that acetylation inhibits hepatic fatty acid oxidation and transport in hens with FLHS, and mainly exerts its effects by affecting protein activity rather than expression. This study provides new nutritional regulation options to alleviate FLHS in laying hens.

MicroR-15b-5p targets JAK2/STAT3 signaling pathway to regulate glucose and lipid metabolism in primary chicken hepatocytes.

Mult omics reveal the mechanism of solid dispersion of genistein in alleviating fatty liver hemorrhagic syndrome in laying hens