Arrb2 causes hepatic lipid metabolism disorder via AMPK pathway based on metabolomics in alcoholic fatty liver

Wu, Dongqing; Yin, Na-Na; Yang, Lei; Chen, Xin; Li, Hai-Di; Li, Xiaofeng; Huang, Cheng; Meng, Xiao‐Ming; Wang, Hua; Li, Jun

doi:10.1042/cs20201363

Cited by 13 publications

(5 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, inhibition of miR-181b-5p enhances protein inhibitor of activated STAT, 1 (PIAS1) in rats with AFL to suppress inflammatory response and oxidative stress [13]. In addition, Arrb2 modulates the Adenosine 5 ′ -monophosphate (AMP)-activated protein kinase (AMPK) pathway to induce dysfunctional hepatic lipid metabolism in AFL [14]. Moreover, Caveolin-1 activates mitophagy to reduce lipid accumulation in AFL through the Pink-1/Parkin pathway [15].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice

2023

Journal of Men's Health

View full text Add to dashboard Cite

Alcoholic liver disease (ALD) is a global liver disease that manifests in a variety of forms, including alcoholic hepatitis, liver inflammation, fatty liver, and liver cirrhosis. One of the early stages of ALD is alcoholic fatty liver (AFL) disease, which is primarily characterized by the accumulation of lipids and inflammation in hepatocytes. Guanylate binding protein 5 (GBP5) has been investigated for its involvement in disease progression. The regulatory effects of GBP5 on the progression of AFL disease are still not well understood. This study aims to investigate the impact of GBP5 on AFL progression and its underlying mechanism of action. To achieve this, gene expression was evaluated using western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR) methods. Lipid accumulation was confirmed using the Oil Red O staining assay, while the levels of Triglyceride (TG), aspartate aminotransferases (AST), and alanine aminotransferases (ALT) were measured using commercial kits. The levels of inflammatory cytokines were assessed using enzyme-linked immuno sorbent assay (ELISA) assay. Finally, cell apoptosis was evaluated using flow cytometry. Cell apoptosis was evaluated through flow cytometry. Our work demonstrated that GBP5 expression was up-regulated in the Ethyl Alcohol (EtOH) group. Additionally, lipid accumulation was increased after EtOH inducement, but this change was attenuated by silencing GBP5. Silencing of GBP5 reduced EtOH-mediated inflammation and cell apoptosis. Finally, it was discovered that knockdown of GBP5 retarded the EtOH-stimulated nuclear factor kappa-B (NF-κB) pathway. Knockdown of GBP5 alleviated lipid accumulation and inflammation in AFL through inhibition of NF-κB pathway. This finding suggested that GBP5 may be a useful bio-target for AFL treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice

2023

Journal of Men's Health

View full text Add to dashboard Cite

show abstract

“…Consistently, silencing β ‐arrestin2 alleviated lipid deposition in AML‐12 cells. This indicates that β ‐arrestin2 promotes hepatic lipid metabolism disorder in alcoholic fatty liver by activating the AMPK signalling pathway (Sun et al, 2021). β ‐Arrestin2 is involved in the pathogenesis of autoimmune hepatitis (AIH), which is characterized by parenchymal inflammation, by inducing inflammation.…”

Section: Role Of β‐Arrestin2 In Diseasesmentioning

confidence: 99%

Insight into the regulatory mechanism of β‐arrestin2 and its emerging role in diseases

Qi,

Chen,

et al. 2024

British J Pharmacology

View full text Add to dashboard Cite

β‐arrestin2, a member of the arrestin family, mediates the desensitization and internalization of most G protein‐coupled receptors (GPCRs) and functions as a scaffold protein in signalling pathways. Previous studies have demonstrated that β‐arrestin2 expression is dysregulated in malignant tumours, fibrotic diseases, cardiovascular diseases and metabolic diseases, suggesting its pathological roles. Transcription and post‐transcriptional modifications can affect the expression of β‐arrestin2. Furthermore, post‐translational modifications, such as phosphorylation, ubiquitination, SUMOylation and S‐nitrosylation affect the cellular localization of β‐arrestin2 and its interaction with downstream signalling molecules, which further regulate the activity of β‐arrestin2. This review summarizes the structure and function of β‐arrestin2 and reveals the mechanisms involved in the regulation of β‐arrestin2 at multiple levels. Additionally, recent studies on the role of β‐arrestin2 in some major diseases and its therapeutic prospects have been discussed to provide a reference for the development of drugs targeting β‐arrestin2.

show abstract

“…Extraction and sample preparation were performed according to a protocol described previously (Sun et al, 2021). Non-targeted metabolite analysis was performed by OE Biotech (Shanghai, China).…”

Section: Liver Metabolomic Analysesmentioning

confidence: 99%

Changes and Correlations of the Intestinal Flora and Liver Metabolite Profiles in Mice With Gallstones

et al. 2021

View full text Add to dashboard Cite

There is increasing appreciation for the roles of the gut-liver axis in liver and gall diseases. Specific gut microbes are associated with susceptibility to gallstone diseases, while the relationship between intestinal flora and liver metabolism in the formation of gallstones remains unclear. In this study, an experimental group of model mice was given a lithogenic diet, and a control group was given a normal diet. Both groups were fed for 8 weeks. Integrating 16S rRNA gene sequencing and non-targeted metabolomics to explore the impact of the lithogenic diet on intestinal flora and liver metabolism, Spearman correlation analysis reveals the network of relationships between the intestine and liver. Our findings showed that the gut microbiome and liver metabolome compositions of the test group were significantly changed compared with those of the normal group. Through our research, biomarkers of gallstones were identified at the phylum (5), class (5), order (5), family (7), and genus levels. We predicted the function of the differential flora. We analyzed the liver metabolism of mice with gallstones paired with their flora, and the results showed that there were 138 different metabolites between the two groups. The metabolic pathways enriched by these differential metabolites are highly consistent with the functions of the disordered flora. We focused on an analysis of the relationship between deoxycholic acid, asymmetric dimethylarginine, glucosamine, tauroursodeoxycholic acid, and the disordered flora. This provides a basis for the establishment of the intestine-liver axis in gallstone disease. This research provides a theoretical basis for the research and development of probiotics and prebiotics.

show abstract

Arrb2 causes hepatic lipid metabolism disorder via AMPK pathway based on metabolomics in alcoholic fatty liver

Cited by 13 publications

References 46 publications

Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice

Knockdown of GBP5 alleviates lipid accumulation and inflammation in alcoholic fatty liver through inhibition of NF-κB pathway in mice

Insight into the regulatory mechanism of β‐arrestin2 and its emerging role in diseases

Changes and Correlations of the Intestinal Flora and Liver Metabolite Profiles in Mice With Gallstones

Contact Info

Product

Resources

About