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<p>Insulin resistance (IR) is a risk factor for numerous metabolic diseases, presenting a significant public health challenge. <i>Smilax china</i> L. polysaccharide (SCP) has been reported to possess anti-obesity properties. However, the effect of SCP on high-fat diet (HFD)-induced IR in mice remains unclear. In this study, a mouse model of HFD-induced IR was established, and SCP intervention was administered. The effects of SCP on IR were comprehensively evaluated using biochemical indicators, histopathological analysis, 16S rRNA sequencing, non-targeted metabolomics analysis, and RT-qPCR analysis. SCP significantly reduced serum glucose and lipid levels while alleviating liver damage. Moreover, SCP remodeled the gut microbiota structure by increasing the relative abundance of <i>Kineothrix</i>, <i>Bacteroides</i>, and <i>Alloprevotella</i>, while suppressing the proliferation of <i>Erysipelatoclostridium</i>, <i>Ruminococcus</i>, and <i>Streptococcus</i>. SCP also elevated the levels of pyridoxal, kynurenine, and lecithin. At the molecular level, SCP upregulated the gene expression of <i>AMPK</i>, <i>PI3K</i>, and <i>AKT</i> in both liver and adipose tissue. In summary, SCP may alleviate HFD-induced IR by modulating the gut microbiota and the AMPK/PI3K/AKT signaling pathway, thereby providing a theoretical basis for SCP-based therapeutic strategies in IR treatment and opening new avenues for the nutritional management of metabolic diseases.</p>

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Smilax china L. Polysaccharide Alleviates HFD-induced Insulin Resistance via Modulating Gut Microbiota and AMPK/PI3K/AKT Signaling Pathway in Mice

  • 期刊论文

  • 发表日期：

    2025年11月14日

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  • Wenjing Wang,
  • Jiaxin Wang,
  • Xinru Hu,
  • Peiqin Chen,
  • Yuqi Cheng,
  • Jingen Li,
  • Guodong Zheng

摘要

Insulin resistance (IR) is a risk factor for numerous metabolic diseases, presenting a significant public health challenge. Smilax china L. polysaccharide (SCP) has been reported to possess anti-obesity properties. However, the effect of SCP on high-fat diet (HFD)-induced IR in mice remains unclear. In this study, a mouse model of HFD-induced IR was established, and SCP intervention was administered. The effects of SCP on IR were comprehensively evaluated using biochemical indicators, histopathological analysis, 16S rRNA sequencing, non-targeted metabolomics analysis, and RT-qPCR analysis. SCP significantly reduced serum glucose and lipid levels while alleviating liver damage. Moreover, SCP remodeled the gut microbiota structure by increasing the relative abundance of Kineothrix, Bacteroides, and Alloprevotella, while suppressing the proliferation of Erysipelatoclostridium, Ruminococcus, and Streptococcus. SCP also elevated the levels of pyridoxal, kynurenine, and lecithin. At the molecular level, SCP upregulated the gene expression of AMPK, PI3K, and AKT in both liver and adipose tissue. In summary, SCP may alleviate HFD-induced IR by modulating the gut microbiota and the AMPK/PI3K/AKT signaling pathway, thereby providing a theoretical basis for SCP-based therapeutic strategies in IR treatment and opening new avenues for the nutritional management of metabolic diseases.