Effects of fatty liver hemorrhagic syndrome on the AMP-activated protein kinase signaling pathway in laying hens

Gao, Xiaona; Liu, Ping; Wu, Cong; Wang, Tiancheng; Liu, Guohui; H, Cao; Zhang, Caiying; Hu, Guoliang; Guo, Xiaomin

doi:10.3382/ps/pey586

Cited by 47 publications

(37 citation statements)

References 31 publications

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“…Gao et al. found that the plasma levels of TG, TCH, LDL, AST, and ALT were significantly increased in the laying hens with FLHS than those in the control group, and HDL was extremely decreased ( Gao et al., 2019 ). In addition, pathological injuries such as steatosis, necrosis and lipid droplet accumulation were observed in liver from FLHS group through HE and oil red O staining.…”

Section: Discussionmentioning

confidence: 99%

“…The hens were raised for 2 wk for acclimatization, and then equally divided into 2 groups: the control group and the FLHS group (n = 10). The hens in FLHS group were induced by the high-energy low-protein diet as described in the previous studies ( Gao et al., 2019 ; Zhuang et al., 2019 ). The detailed composition of the diets for the hens was shown in Supplementary Table 1 .…”

Section: Methodsmentioning

confidence: 99%

“…The common pathologic features of FLHS and NAFLD are excess hepatic lipid deposition. Previous studies have provided that pathogenic causes such as inflammation, lipid disorder, oxidative stress, autophagy, and gut microbiota are related to FLHS ( Gao et al., 2019 ; Xing et al., 2020 ). However, the exact pathogenesis underlying FLHS have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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

Meng

Liu

et al. 2021

Poultry Science

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As a metabolic disease, fatty liver hemorrhagic syndrome ( FLHS ) has become the major factor responsible for the noninfectious cause of mortality in laying hens, which lead to huge economic losses to poultry industry. However, the pathogenesis of FLHS remains unclear. The aim of present study was to identify novel liver metabolites associated with FLHS. Twenty healthy Chinese commercial Jing Fen laying hens aged 90 d were used in present study. After acclimatization for 2 wk, the hens were divided into 2 treatments (n = 10): control group (normal diet) and FLHS group (high-energy low-protein diet). The experiment lasted for 48 d, and the laying hens were killed for blood and liver sampling at the end of the experiment. Blood biochemical indicators and liver pathological changes were examined. Meanwhile, the changes in liver metabolic profile were investigated with the application of metabolomics approach. Significant increased levels of alanine aminotransferase, aspartate aminotransferase, low density lipoprotein, total cholesterol and triglycerides, decreased high density lipoprotein ( P < 0.01), and hepatic steatosis were observed in hens of FLHS group, which suggested FLHS was successfully established in this study. Distinct changes in metabolite patterns in liver between control and FLHS group were observed by partial least-squares discriminant analysis. In total, 42 liver metabolites including tyrosine, glutathione, carnitine, linoleic acid, uric acid, arachidonic acid ( ARA ), lactate and lysophosphatidylcholine (14: 0) were identified and considered to be related with pathogenesis of FLHS. Pathway analysis revealed that these metabolites were mainly involved in amino acid metabolism, fatty acid metabolism, ARA metabolism, glucose metabolism and glycerophospholipid metabolism. Furthermore, targeted metabolomics found that ARA metabolites such as prostaglandins and hydroxyeicosatetraenoic acids were significantly increased in FLHS group ( P < 0.05). In conclusion, our data showed that liver metabolites and ARA metabolism were linked to the pathophysiology of FLHS, which provided a basis for understanding the pathogenesis of FLHS in laying hens.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Meng

Liu

et al. 2021

Poultry Science

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“…Hens fed a HF diet [4][5][6][7] or HFLP diet [1,[9][10][11][12] have been created for studying the pathogenesis of FLHS in laying hens or as a model for human NAFLD investigation. The pathological characters of FLHS include hepatic fat accumulation in the liver with hemorrhage or rupture.…”

Section: Discussionmentioning

confidence: 99%

“…It is associated with approximately 40% of the necropsied hens, and can be up to 74% in the caged laying hens [2]. Several factors have been relate to FLSH, such as nutritional, metabolic, hormonal, environmental, and genetic factors [1,2], but excess energy intake is the fundamental player as FLHS can be induced by a high-fat diet (HFD) [4][5][6][7][8] or a high fat and low protein (HFLP) diet [1,[9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

Zou

et al. 2020

Preprint

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Background: Osteocalcin (OCN), as an energy-regulating hormone, involves in preventing nonalcoholic steatohepatitis. Laying hens have been used as an animal model for investigating liver function and related metabolic disordersas that the synthesis of fat in laying hens is much faster than in mammals with limited adipose tissue. The aim of this study was to investigate the effects of OCN on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Methods: Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of three treatments: normal diet (ND + vehicle , ND+V), high-fat diet (HFD + vehicle, HFD+V), and HFD + OCN (3 μg/bird, 1 time/2 days, i.m.) for 40 days. At experimental day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor Necrosis Factor-alpha (TNF-α) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by Real-time PCR. And oxidative stress was evaluated using Malondialdehyde (MDA) and Glutathione peroxidase (GSH-Px) assay kits. Results: The results showed HFD hens had more severe liver haemorrhage and fibrosis than ND hens. The ultra-microstructural examination showed that hepatocytes of HFD hens appeared necrotic pyknosis associated with great intracellular electron, mitochondrial swelling, shrunk nucleus and absence of autolysosomes. OCN mitigated these pathological changes by improved HFD hens’ insulin resistance via alleviating the glucose intolerence and improving insulin sensitivity; inhibited HFD-induced oxidative stress as evidenced by decreased liver concentrations of MDA but increased GSH-Px; and reduced the inflammatory reaction with reducing blood IL-6 and TNF-α concentrations and mRNA expressions. Conclusion: These results suggest a high-fat diet promotes the FLHS development in aged hens, while OCN prevents the FLHS process through inhibiting insulin resistance, inflammatory reaction, oxidative stress and fibrosis, and acting autophagy.

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Development of fatty liver disease model using high cholesterol and low choline diet in white leghorn chickens

Yadav,

Boley,

Khatiwada

et al. 2024

Vet Res Commun

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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.

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Effects of fatty liver hemorrhagic syndrome on the AMP-activated protein kinase signaling pathway in laying hens

Cited by 47 publications

References 31 publications

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

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

Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

Development of fatty liver disease model using high cholesterol and low choline diet in white leghorn chickens

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