IDDF2021-ABS-0197 Delayed intervention of agaropectin-derived oligosaccharides alleviate lipid accumulation by modulating intestinal flora homeostasis

Abstract Background:Carbon black nanoparticles (CBNPs) are a major carbonaceous nanomaterial, which have been widely left in the environment. The integrity of the gut-liver axis function is critical to the survival of animals. Therefore, we studied the effects of three concentrations of CBNPs (50, 100, 200 mg/L) on zebrafish intestines, liver and intestinal flora. Results:The results showed that CBNPs exposure could reduce the diversity of intestinal flora, change the structure of core microbial populations, enhance the permeability of the intestinal mucosal barrier, and cause changes in genes related to tight junctions in intestinal tissues. The H&E staining and Oil red O staining showed that CBNPs exposure would lead to vacuolar degeneration and lipid accumulation in zebrafish liver. Further detection of glycolipid metabolism related genes showed that CBNPs exposure induced the up-regulation of glycolysis related genes PFKFB3, LDHA, and LEPr, reduces the expression of glycogen synthase kinase GSK-3b, and increases lipid transport and production related genes PPAR-α, PPAR-γ, LIPC, apoa4, Fabp2 and Fabp11 expression. Conclusions:In brief, our data demonstrated that CBNPs exposure induced intestinal microflora disturbance in zebrafish can lead to liver lipid accumulation.

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Carbon Black Nanoparticles Exposure Induces Intestinal Flora Dysbiosis and Consequent Activation of Gut-liver Axis Leading to Liver Lipid Accumulation in Zebrafish

10.21203/rs.3.rs-792204/v1 ◽

2021 ◽

Author(s):

Qingqing Liu ◽

Bing Wang ◽

Shengchen Wang ◽

Hongyuan Jing ◽

Shiwen Xu

Keyword(s):

Lipid Accumulation ◽

Glycogen Synthase ◽

Liver Lipid ◽

Intestinal Flora ◽

Mucosal Barrier ◽

Vacuolar Degeneration ◽

Glycolipid Metabolism ◽

Ppar Γ ◽

Carbon Black Nanoparticles ◽

Carbonaceous Nanomaterial

Abstract BackgroundCarbon black nanoparticles (CBNPs) are a major carbonaceous nanomaterial, which have been widely left in the environment. The integrity of the gut-liver axis function is critical to the survival of animals. Therefore, we studied the effects of three concentrations of CBNPs (50, 100, 200 mg/L) on zebrafish intestines, liver and intestinal flora. ResultsThe results showed that CBNPs exposure could reduce the diversity of intestinal flora, change the structure of core microbial populations, enhance the permeability of the intestinal mucosal barrier, and cause changes in genes related to tight junctions in intestinal tissues. The H&E staining and Oil red O staining showed that CBNPs exposure would lead to vacuolar degeneration and lipid accumulation in zebrafish liver. Further detection of glycolipid metabolism related genes showed that CBNPs exposure induced the up-regulation of glycolysis related genes PFKFB3, LDHA, and LEPr, reduces the expression of glycogen synthase kinase GSK-3b, and increases lipid transport and production related genes PPAR-α, PPAR-γ, LIPC, apoa4, Fabp2 and Fabp11 expression. ConclusionsIn brief, our data demonstrated that CBNPs exposure induced intestinal microflora disturbance in zebrafish can lead to liver lipid accumulation.

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TMAO Stimulate Inflammation and Lipid Accumulation via NF-κB Signaling Pathway in Nonalcoholic Fatty Liver Disease

10.21203/rs.3.rs-993103/v1 ◽

2021 ◽

Author(s):

zhijun chen ◽

Jiale Zhang ◽

Qian Cheng ◽

Xiangsheng Cai ◽

RuiTian Xie ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Signaling Pathway ◽

Lipid Accumulation ◽

Fatty Liver Disease ◽

Intestinal Flora ◽

Common Disease ◽

Nonalcoholic Fatty Liver

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is a common disease and it is commonly associated with obesity. Trimethylamine N-oxide (TMAO) is a metabolite of intestinal flora generated in liver by flavin-containing monooxygenase 3 (FMO3), which has been widely studied in cardiovascular diseases and obesity. However, the mechanism of TMAO reacted on liver remains unclear. This study aimed to determine TMAO activated hepatitis inflammation and lipid accumulation which was associated with nuclear factor kappa B (NF-κB) signaling pathway in vitro. ResultsThe present study showed that TMAO in 50μM markedly increased the LO2 cells function and decreased the cells inflammation. However, over the concentration of 200μM in TMAO, cells inflammation was increased and function was declined apparently. In addition, TMAO promoted lipid accumulation. Mechanistically, this change was accompanied by the activation of NF-κB signaling pathway. Furthermore, blocking NF-κB by SN50 was significantly increased in lipid accumulation and apoptosis. SN50 was markedly decreased the protein expression stimulating by TMAO.ConclusionsOverall, the result suggested that TMAO promotes cells inflammation and lipid accumulation in hepatocytes and it might be associated with NF-κB signaling pathway.

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