Abstract

Potentilla discolor Bunge (PDB), a perennial herb, has been used as a traditional Chinese medicine in the therapy of many diseases. The aim of the current study was to investigate the effect of PDB water extract on systemic inflammation and gut microbiota in type 2 diabetic (T2D) mice induced by high-fat diet (HFD) and streptozotocin (STZ) injection. C57BL/6J mice were randomly divided into a normal diet (ND) group, T2D group, and PDB group (diabetic mice treated with PDB water extract at a dose of 400 mg/kg body weight). Results showed that PDB significantly decreased the levels of lipopolysaccharide (LPS) and pro-inflammatory cytokines in serum. Further investigation showed that PDB significantly reduced the ratio of Firmicutes/Bacteroidetes and the relative abundance of Proteobacteria in fecal samples of diabetic mice. In addition, PDB notably alleviated intestinal inflammation as evidenced by decreased expression of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-κB (NF-κB), and inflammatory cytokines. PDB also reversed the decreased expression of intestinal mucosal tight junction proteins including Claudin3, ZO-1, and Occludin. Meanwhile, the levels of fecal acetic acid and butyric acid and their specific receptors including G-protein-coupled receptor (GPR) 41 and 43 expression in the colon were also increased after PDB treatment. Our results indicated that PDB might serve as a potential functional ingredient against diabetes and related inflammation.

Highlights

  • Type 2 diabetes (T2D), a chronic systemic progressive metabolic disease, is characterized by hyperglycemia and chronic low-grade inflammation

  • The present study aimed to explore the impact of Potentilla discolor Bunge (PDB) on the gut microbiota and inflammation status of diabetic mice induced by high-fat diet (HFD) and streptozotocin (STZ)

  • In attempt to investigate the effects of PDB on endotoxemia and inflammation in diabetic mice, the levels of LPS and inflammatory cytokines including tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 were measured

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Summary

Introduction

Type 2 diabetes (T2D), a chronic systemic progressive metabolic disease, is characterized by hyperglycemia and chronic low-grade inflammation. Gut microbiota is a complex community of bacteria residing in the gastrointestinal tract, which usually maintains a mutually beneficial relationship with its host [1]. The gut barrier is an indispensable structure to avoid the excessive translocation of LPS into the circulation system, thereby maintaining a mutually beneficial relationship between gut bacteria and host. Oral ingestion of Akkermansia muciniphila, an intestinal mucin-degrading bacterium, enhanced glucose tolerance and alleviated white adipose tissue inflammation in high-fat diet (HFD) fed mice [7]. All this evidence suggests that gut microbiota might be a promising and feasible target for T2D treatment

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