Mitigative effect of natural resistant starch from kudzu on intestinal-hepatic injury in mice exposed to high-fat diet and dextran sulfate sodium.

Abstract

Non-alcoholic fatty liver disease (NAFLD) has become a globally prevalent metabolic disorder, with its pathogenesis closely linked to dysfunction of the gut-liver axis. In this study, a mouse model of NAFLD was established by a high-fat diet (HFD) combined with dextran sulfate sodium (DSS), and was intervened with resistant starch derived from Kudzu (P-RS). The results demonstrated that P-RS supplementation significantly alleviated hepatic steatosis in NAFLD mice. Specifically, P-RS reduced serum levels of inflammatory mediators, including tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6), as well as biochemical markers such as total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Additionally, P-RS decreased the intestinal permeability marker lipopolysaccharide (LPS) while upregulating the expression of tight junction proteins, including zonula occludens-1 (ZO-1), and claudin-1, thereby enhancing intestinal barrier integrity. Furthermore, P-RS promoted the proliferation of beneficial gut bacteria, such as norank_f__Eubacterium_coprostanoligenes_group, Lachnospiraceae_NK4A136_group, Colidextribacter and unclassified_f__Lachnospiraceae. It also modulated bile acid metabolism by elevating the levels of hyodeoxycholic acid (HDCA) and deoxycholic acid (DCA), which ultimately suppressed hepatic lipid synthesis and inflammatory responses. These findings collectively suggest that P-RS exerts protective effects against NAFLD by modulating the gut-liver axis.