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Effect of deficiency of NLRP6 on hepatic lipids accumulation during non-alcoholic fatty liver disease in mice.

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is one of the main causes of liver diseases in the world. At present, the pathogenesis of NAFLD is not completely clear, and the regulatory role of inflammatory corpuscles in NAFLD-related metabolic diseases is increasingly prominent. NLRP6 is a member of the NLRs family of pattern recognition receptors and is related to the occurrence and development of NAFLD, but the specific mechanism is still unclear. We report here that NLRP6 is an important regulator of liver lipid metabolism, and its absence will affect the formation and accumulation of lipid droplets in the liver. In the HFD-induced NAFLD model group, NLRP6 deletion increased the mouse lipid content and aggravated hepatocyte steatosis by up-regulating the expressions of ADRP and CIDEC and down-regulating the expression of ApoB100.On the contrary, overexpression of NLRP6 in hepatocytes can significantly reduce intracellular lipid content and lipid droplets, and reduce the expression of ADRP and CIDEC. Indicated that NLRP6 can inhibit the accumulation of lipid droplets in hepatocytes by regulating the expression of ADRP, CIDEC and ApoB100, and thus alleviating the symptoms of NAFLD.

ORGANISM(S): Mus musculus

PROVIDER: GSE239747 | GEO | 2024/01/31

REPOSITORIES: GEO

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Project description:Objective: Nonalcoholic fatty liver disease (NAFLD) is linked to obesity and diabetes, suggesting an important role of adipose tissue in the pathogenesis of NAFLD. Here we aim to investigate the interaction between adipose tissue and liver in NAFLD, and identify potential early plasma markers that predict NASH. Research Design and Methods: C57Bl/6 mice were chronically fed a high fat diet to induce NAFLD and compared with mice fed low fat diet. Extensive histological and phenotypical analyses coupled with a time-course study of plasma proteins using multiplex assay was performed. Results: Mice exhibited pronounced heterogeneity in liver histological scoring, leading to classification into 4 subgroups: LF-low (LFL) responders displaying normal liver morphology, LF-high (LFH) responders showing benign hepatic steatosis, HF-low (HFL) responders displaying pre-NASH with macrovesicular lipid droplets, and HF-high (HFH) responders exhibiting overt NASH characterized by ballooning of hepatocytes, presence of Mallory bodies, and activated inflammatory cells. Compared to HFL responders, HFH mice gained weight more rapidly and exhibited adipose tissue dysfunction characterized by decreased final fat mass, enhanced macrophage infiltration and inflammation, and adipose tissue remodelling. Plasma haptoglobin, IL-1β, TIMP-1, adiponectin and leptin were significantly changed in HFH mice. Multivariate analysis indicated that in addition to leptin, plasma CRP, haptoglobin, eotaxin and MIP-1α early in the intervention were positively associated with liver triglycerides. Intermediate prognostic markers of liver triglycerides included IL-18, IL-1β, MIP-1γ and MIP-2, whereas insulin, TIMP-1, GCP-2 and MPO emerged as late markers. Conclusions: Our data support the existence of a tight relationship between adipose tissue dysfunction and NASH pathogenesis and point to several novel potential predictive biomarkers for NASH. Keywords: Expression profiling by array Male wildtype C57Bl/6 mice were fed LFD or HFD for 21 weeks. Mice were divided into 4 groups based on liver histology.

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Effect of deficiency of NLRP6 on hepatic lipids accumulation during non-alcoholic fatty liver disease in mice.

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