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<p>Probiotic supplementation was a novel therapeutic approach for treating metabolic related diseases via “gut-liver” axis. However, the effect of <i>Clostridium butyricum</i> (<i>CB</i>) supplementation on type 2 diabetes mellitus (T2DM)-associated steatohepatitis was unknown. This study revealed that <i>CB</i> alleviated liver damage and hepatitis in 18 weeks-old <i>db/db</i> mice. Targeted metabolomics analysis showed that the dysregulated short chain fatty acids (SCFAs) metabolism homeostasis was regained by <i>CB</i> in the colon content of <i>db/db</i> mice, especially butyric acid. Treatment with sodium butyrate (NaB) significantly attenuated steatosis, inflammation, and fibrosis of <i>db/db</i> mice, and high glucose (HG) and free fatty acid (FFA) co-treated HepG2 cells. In-depth mechanism research suggested that the hepatoprotective effects of <i>CB</i> on T2DM was associated with the suppression of IκB-α/β-arrestin2/NF-κB signaling pathway via intestinal butyrate-medicated hepatic Takeda G-protein-coupled receptor 5 (TGR5). Overall, our results demonstrated a potential novel mechanism for <i>CB</i> as effective nutritional intervention for T2DM-related steatohepatitis via “gut-liver” axis.</p>

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Role of intestinal SCFAs homeostasis in the hepatoprotective effect of Clostridium butyricum in T2DM

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月11日

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  • Meng Yan,
  • Dandan Pan,
  • Libang Chen,
  • Jiale Pang,
  • Yuting Shao,
  • Qian Cheng,
  • Ying Liu,
  • Zeyuan Yin,
  • Zhenzhou Jiang,
  • Pian Sha,
  • Yuqian Huang,
  • Yilin Fan,
  • Sitong Qian,
  • Tao Wang,
  • Qian Lu,
  • Tingting Yang

摘要

Probiotic supplementation was a novel therapeutic approach for treating metabolic related diseases via “gut-liver” axis. However, the effect of Clostridium butyricum (CB) supplementation on type 2 diabetes mellitus (T2DM)-associated steatohepatitis was unknown. This study revealed that CB alleviated liver damage and hepatitis in 18 weeks-old db/db mice. Targeted metabolomics analysis showed that the dysregulated short chain fatty acids (SCFAs) metabolism homeostasis was regained by CB in the colon content of db/db mice, especially butyric acid. Treatment with sodium butyrate (NaB) significantly attenuated steatosis, inflammation, and fibrosis of db/db mice, and high glucose (HG) and free fatty acid (FFA) co-treated HepG2 cells. In-depth mechanism research suggested that the hepatoprotective effects of CB on T2DM was associated with the suppression of IκB-α/β-arrestin2/NF-κB signaling pathway via intestinal butyrate-medicated hepatic Takeda G-protein-coupled receptor 5 (TGR5). Overall, our results demonstrated a potential novel mechanism for CB as effective nutritional intervention for T2DM-related steatohepatitis via “gut-liver” axis.