Abstract
Our previous studies have shown that chlorogenic acid (CGA) could significantly improve acute and chronic liver injury through antioxidant and anti-inflammatory activities. However, its effect on non-alcoholic fatty liver disease (NAFLD) are not entirely clear. This study aims to explore the effect of CGA on NAFLD induced by high-fat diet (HFD) and whether it regulates the gut microbiota and Glucagon-like peptide-1 (GLP-1). NAFLD mice were established by HFD and treated with or without CGA. Serum transaminase, fasting blood glucose (FBG), blood lipids, insulin, GLP-1 and lipopolysaccharide (LPS) were detected. Liver histology was evaluated with Hematoxylin-eosin staining. Toll like receptor 4 (TLR4) signaling pathway was analyzed with western blot and inflammatory cytokines were detected with real-time PCR. The content of gut microbiota were determined with real-time PCR of the bacterial 16S rRNA gene. Expressions of intestine tight junctional protein were examined with immunohistochemistry. CGA could alleviate HFD-induced hepatic steatosis and inflammation, reduce serum transaminase, FBG and blood lipids, increase insulin sensitivity. CGA also could reverse HFD-induced activation of TLR4 signaling pathway and expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in liver. Meanwhile, CGA increased the content of Bifidobacterium and reduced the content of Escherichia coli in feces. Furthermore, CGA could increase the expression of tight junction proteins Occludin and zonula occludens-1 (ZO-1) in intestinal tissue. Moreover, CGA could the level of LPS and increased the level of GLP-1 in portal vein. These results indicated that CGA protected against HFD-induced hepatic steatosis and inflammation probably through its anti-inflammatory effects associated with regulation of gut microbiota and an increase of GLP-1 secretion and thus could be used as a potential drug for prevention and treatment of NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) has become the world’s most common chronic liver disease and is the main cause of end-stage liver disease (Mikolaevi et al, 2021)
Overgrowth of the gut microbiota promotes the development of obesity and insulin resistance, which can damage the intestinal mucosa barrier function and allow endotoxins to travel to the liver, where they can induce or exacerbate liver inflammation and oxidative stress damage, leading to occurrence and progression of hepatic steatosis, inflammation and fibrosis (Akash et al, 2019)
This study aims to explore the effect of chlorogenic acid (CGA) on non-alcoholic fatty liver disease (NAFLD) induced by high-fat diet (HFD) and whether it regulates the gut microbiota and Glucagon-like peptide-1 (GLP-1)
Summary
Non-alcoholic fatty liver disease (NAFLD) has become the world’s most common chronic liver disease and is the main cause of end-stage liver disease (Mikolaevi et al, 2021). It is generally believed that NAFLD is associated with abnormal glucose and lipid metabolism, insulin resistance, inflammation, oxidative stress and imbalanced gut microbiota. Revealing the pathogenesis of NAFLD and finding more effective therapeutic targets and drugs are challenges in the field of fatty liver research. Gut microbiota imbalance participates in the occurrence and development of NAFLD (Aron-Wisnewsky et al, 2020). Overgrowth of the gut microbiota promotes the development of obesity and insulin resistance, which can damage the intestinal mucosa barrier function and allow endotoxins to travel to the liver, where they can induce or exacerbate liver inflammation and oxidative stress damage, leading to occurrence and progression of hepatic steatosis, inflammation and fibrosis (Akash et al, 2019)
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