Lonicerae flos polysaccharides improve nonalcoholic fatty liver disease by activating the AMPK pathway and reshaping gut microbiota

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver cirrhosis and cancer. Lonicerae flos polysaccharides (LPs) have been shown to be effective in treating metabolic diseases; however, the therapeutic effects and underlying molecular mechanisms of LPs in NAFLD remain unclear. To investigate the morphological characterization of Lonicerae flos polysaccharides (LPs) and the mechanism of LPs in relieving nonalcoholic fatty liver disease (NAFLD). The morphology of LPs was observed using a atomic force microscope (AFM), X-ray diffraction (XRD) spectrum, thermal weight (TG) and thermal weight derivative (DTG); NAFLD mice were treated with LPs at the same time as they were induced by western diet, and then the indexes related to glycolipid metabolism, fibrosis, inflammation, and autophagy in the serum and liver of the mice were detected. The atomic force microscope analysis results indicated that the LPs displayed sugar chain aggregates, exhibited an amorphous structure; and relatively stable in thermal cracking at 150 °C. We also found that LPs exerted therapeutic effects in NAFLD. The LPs prevented high-fat and -cholesterol diet-induced NAFLD progression by regulating glucose metabolism dysregulation, insulin resistance, lipid accumulation, inflammation, fibrosis, and autophagy. AMPK inhibitor compound C abrogated LP-induced hepatoprotection in mice with NAFLD. The LPs further treated NAFLD by reshaping the structure of the gut microbiota, in which an increase in the amount of Desulfovibrio bacteria within the gut. LPs exert protective effects against NAFLD in mice with by improving the structure of the intestinal flora and activating the AMPK signaling pathway. This article is protected by copyright. All rights reserved.