Corticosterone-Induced Lipogenesis Activation and Lipophagy Inhibition in Chicken Liver Are Alleviated by Maternal Betaine Supplementation

Hu, Yun; Sun, Qinwei; Hu, Yan; Hou, Zhen; Zong, Yibo; Omer, Nagmeldin A.; Abobaker, Halima

doi:10.1093/jn/nxx073

Cited by 29 publications

(33 citation statements)

References 58 publications

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“…Plasma activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and the levels of triglycerides (TG), total cholesterol (TCHOL), high-and low-density lipoprotein cholesterol (HDL and LDL, respectively), and glucose (GLU) were analyzed using an automatic biochemical analyzer (7020, HITACHI, Tokyo, Japan), as previously described [22]. Hepatic triglycerides were measured using a tissue triglyceride assay kit (E1013; Applygen Technologies Inc., Beijing, China) as previously described [8].…”

Section: Plasma Biochemical Indicators Measurement and Triglycerides mentioning

confidence: 99%

“…It has been demonstrated that excessive glucocorticoid (GC) exposure can cause metabolic syndrome, including fatty liver disease, in both mammals and birds [7]. The active form of GC in chickens is primarily corticosterone (CORT), an indicator of stress [8]. Moreover, it is well known that treatment with exogenous CORT can cause abnormal fat deposition in the liver [9,10].…”

Section: Introductionmentioning

confidence: 99%

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Hepatic Inflammatory Response to Exogenous LPS Challenge is Exacerbated in Broilers with Fatty Liver Disease

Mei

Hao

Xie

et al. 2020

Animals

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This study aimed to examine hepatic function and inflammatory response in broilers with fatty livers, following acute lipopolysaccharide (LPS) challenge. One-day-old Lihua yellow broilers were fed a basal diet. Broilers were divided into four groups: control (CON), corticosterone treatment (CORT), LPS treatment (LPS), and LPS and CORT treatment (LPS&CORT). Results show that CORT induced an increase in plasma and liver triglycerides (TGs), which were accompanied by severe hepatic steatosis. The LPS group showed hepatocyte necrosis with inflammatory cell infiltration. Total liver damage score in the LPS&CORT group was significantly higher than that in the LPS group (p < 0.05). Activity levels of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were similar in the CON and CORT groups, but higher in the LPS group. Gene expression upregulation of the proinflammatory cytokines (NF-κB, IL-1β, IL-6, IFN-γ, and iNOS) was also noted in the LPS group (p < 0.05). In particular, LPS injection exacerbated the gene expression of these proinflammatory cytokines, even when accompanied by CORT injections (p < 0.05). In summary, our results indicate that broilers suffering from fatty liver disease are more susceptible to the negative effects of LPS, showing inflammatory response activation and more severe damages to the liver.

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Section: Plasma Biochemical Indicators Measurement and Triglycerides mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hepatic Inflammatory Response to Exogenous LPS Challenge is Exacerbated in Broilers with Fatty Liver Disease

Mei

Hao

Xie

et al. 2020

Animals

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“…Therefore, controlling lipid accumulation in the liver can prevent the progression of lipid metabolic disorders [22]. In this study, fatty liver disease was mimicked in broilers by consecutive injection of CORT, showing with the typical characteristics of fatty liver disease as the previous report [10]. However, our results showed that probiotics supplementation from post-hatching for 2 weeks could effectively protect the lost of body weight, and prevent the progress of fatty liver disease induced by CORT in broilers.…”

Section: Discussionmentioning

confidence: 45%

“…However, our results showed that probiotics supplementation from post-hatching for 2 weeks could effectively protect the lost of body weight, and prevent the progress of fatty liver disease induced by CORT in broilers. It's reported that chronic CORT treatment reduces protein synthesis but promotes protein degradation, and nally leading to the loss of body weight in chickens [10,23]. It has been described that probiotic exhibits bene cial effect on body weight gain [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…Glucocorticoid hormones (GCs) are important regulators of lipid metabolism, promoting lipogenesis when treated with chronic exposure [5].For instance, chronic excessive GCs exposure induced whole-body insulin resistance, strongly related to metabolic dysfunction including intrahepatic lipid accumulation, intramuscular fat deposition and abdominal adiposity in humans [6,7].Corticosterone (CORT) is the main active form of GC in chickens. Previous studies have shown that fatty liver disease can be induced by excessive CORT exposure in broilers [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Probiotics Supplementation Alleviate Corticosterone-induced Fatty Liver Disease Related With the Changes of Hepatic Lipogenesis and Gut Microbiota Profile in Broiler

Mei

Feng

Yao

et al. 2020

Preprint

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Background:Emerging evidencesindicate a close relationship between gut microbiotaand fatty liver disease.It has been suggested that gut microbiota modulation with probiotics improved fatty liver disease in rodents and human, yet it still remains unclear in poultry.Results: Ninety six one-day-old green-legged chicken were divided into control group (CON) and probiotic group (PB), respectively. Probiotics were administrated throughdrinking water for two weeks from 1-day-old. At 28 d of age,16 broilers selectedfromCON or PB group randomly, and receivedvehicle(15% ethanol) or CORT(4.0 mg/kg)treatmentdaily viasubcutaneous injection for a week to induce fatty liver. At the end of the experiment, broilers from 4 groups,control group(CON), corticosterone group (CORT), probiotic group (PB), PB plusCORT group(CORT&PB),were slaughtered for sampling and analysis.The results showed that probiotics administration significantly prevented CORT-induced body weight loss(P<0.05), but did not alleviate the reduction of immune organs weight caused by CORT. Compared to CON,broilers in CORT group exhibited a significant increase of triglyceride (TG) levelin both plasma and liver(P< 0.01), as well as severe hepatocytic steatosis and hepatocellular ballooning, and accompanied with the up-regulation of hepatic lipogenesis genes expression. However, probiotics supplementation markedly decreased the intrahepatic lipid accumulation and steatosis histological score, which was associated withthedown-regulation of sterol regulatory element-binding protein-1 (SREBP1) and acetyl-CoA carboxylase (ACC) mRNA (P< 0.05)as well as it protein (P= 0.06) expression.Cecal microbiota composition was determined by 16S rRNA high-throughput sequencing. Results showed that CORT treatment induced distinct gut microbiota alterations with a decrease of microbial diversity, and anincrease of proteobacteriaabundance (P<0.05). On the contrary, probiotic supplementation increased the beta diversity and increased community richness and diversity index(P> 0.05), as well as the abundance of Intestinimonas(P<0.05).Conclusion: Our results indicate that CORT treatment induced serious fatty liver disease and altered the gut microbiota composition in broilers, however,probiotics supplementation from post-hatching had a beneficial effect on alleviatingfatty liver disease through regulating lipogenic genes expression and increasing gut microbiota diversity andbeneficial bacteria abundanceimbalance.

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Chronic corticosterone exposure induces liver inflammation and fibrosis in association with m6A-linked post-transcriptional suppression of heat shock proteins in chicken

Feng

Hou

et al. 2020

Cell Stress and Chaperones

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Our previous study had shown that chronic corticosterone (CORT) exposure causes excessive fat deposition in chicken liver, yet it remains unknown whether it is associated with inflammation and fibrosis. In general, heat shock proteins (HSPs) are activated in response to acute stress to play a cytoprotective role, and this activation is associated with m 6 A-mediated post-transcriptional regulation. However, changes of HSPs and the m 6 A methylation on their mRNAs in response to chronic CORT treatment in chicken liver have not been reported. In this study, chronic CORT exposure induced inflammation and fibrosis in chicken liver, associated with significantly modulated expression of HSPs that was significantly upregulated at mRNA level yet downregulated at protein level. Concurrently, m 6 A methyltransferases METTL3 content was upregulated together with the level of m 6 A methylation on HSPs transcripts. The m 6 A-seq analysis revealed 2-6 significantly (P < 0.05) hypermethylated m 6 A peaks in the mRNA of 4 different species of HSPs in CORT-treated chicken liver. HSP90B1 transcript had 6 differentially methylated m 6 A peaks among which peaks on exon 16 and exon 17 showed 3.14-and 4.72-fold of increase, respectively. Mutation of the 8 predicted m 6 A sites on exon 16 and exon 17 resulted in a significant (P < 0.05) increase in eGFP-fused content of HSP90B1 exon 16 and exon 17 fragment in 293 T cells, indicating a possible role of m 6 A in post-transcriptional regulation of HSPs. In conclusion, chronic CORT exposure induces inflammation and fibrosis in chicken liver along with an increase in the levels and m6A methylation of several HSPs mRNAs; HSPs levels were however reduced under the indicated conditions. Results presented suggest that the reduction in HSPs levels may be associated with m6A methylation in CORT-exposed chickens.

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Corticosterone-Induced Lipogenesis Activation and Lipophagy Inhibition in Chicken Liver Are Alleviated by Maternal Betaine Supplementation

Abstract: These results indicate that maternal betaine supplementation protects male juvenile chickens from CORT-induced TG accumulation in the liver via epigenetic modulation of lipogenic and lipophagic genes.

Cited by 29 publications

References 58 publications

Hepatic Inflammatory Response to Exogenous LPS Challenge is Exacerbated in Broilers with Fatty Liver Disease

Hepatic Inflammatory Response to Exogenous LPS Challenge is Exacerbated in Broilers with Fatty Liver Disease

Probiotics Supplementation Alleviate Corticosterone-induced Fatty Liver Disease Related With the Changes of Hepatic Lipogenesis and Gut Microbiota Profile in Broiler

Chronic corticosterone exposure induces liver inflammation and fibrosis in association with m6A-linked post-transcriptional suppression of heat shock proteins in chicken

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