香港大学:三七皂苷通过菌群-脂肪互作,抵抗肥胖
  • 三七总皂苷(PNS)能帮助食源性肥胖(DIO)小鼠抵抗肥胖;
  • PNS改变DIO小鼠的肠道菌群,增加AKK菌和狄氏副拟杆菌的丰度,粪菌移植和抗生素处理试验表明菌群介导了PNS的抗肥胖作用;
  • PNS诱导的菌群通过激活瘦素介导的AMPKα/STAT3信号通路,促进小鼠棕色脂肪产热和白色脂肪米色化,发挥抗肥胖作用;
  • 在缺乏瘦素的ob/ob小鼠中,PNS诱导的肠道菌群对白色脂肪产热和褐化无明显影响,证明瘦素在其中发挥关键介导作用。
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香港大学Yibin Feng团队研究成果。文章结合动物模型和细胞模型,研究在三七总皂苷(PNS)的干预下,菌群-脂肪互作过程中瘦素发挥的作用。研究结果显示,PNS通过促进脂肪生热和白色脂肪褐化,发挥抗肥胖作用,与瘦素-AMPKα/STAT3信号通路活化有关。
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Theranostics [IF:8.579]

Panax notoginseng saponins modulate the gut microbiota to promote thermogenesis and beige adipocyte reconstruction via leptin-mediated AMPKα/STAT3 signaling in diet-induced obesity

在膳食诱导的肥胖中,三七总皂苷调节肠道菌群并通过瘦素介导的AMPKα/STAT3信号传导,促进热生成和米色脂肪细胞重建

10.7150/thno.47746

2020-09-14, Article

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Background: Activation of the thermogenic program in white and brown adipocytes presents a promising avenue for increasing energy expenditure during the treatment of obesity. The endogenous mechanism for promoting thermogenesis in brown adipocytes or browning in white adipocytes has indicated that the gut microbiota is a crucial regulator of the host energy balance. However, whether the effects of the therapeutic intervention-induced modulation of the gut microbiota on adipocyte browning involved the regulation of leptin remains unclear.
Method: The adipose features were analyzed by body composition analysis, infrared camera observations, transmission electron microscopy and H&E staining. The gene and protein expression in adipose tissue were detected by qRT-PCR, immunoblotting, immunohistochemistry and immunofluorescence staining. The gut microbiome signature was identified by 16S rRNA gene amplicon sequencing, and both mice with high-fat diet-induced obesity (DIO) and mice with antibiotics-induced microbiome depletion were subjected to fecal microbiota transplantation.
Results: Treatment with Panax notoginseng saponins (PNS) shaped the murine gut microbiome by increasing the abundances of Akkermansia muciniphila and Parabacteroides distasonis, and as a result, DIO mice harbored a distal gut microbiota with a significantly increased capacity to reduce host adiposity. The PNS-induced modulation of the gut microbiota in DIO mice could increase brown adipose tissue (BAT) thermogenesis and beige adipocyte reconstruction by activating the leptin-AMPK/STAT3 signaling pathway, which results in the promotion of energy expenditure. Leptin has an essential influence on the anti-obesity effects of PNS. In cases of leptin deficiency, the PNS-induced modulation of the gut microbiota exerts negative effects on thermogenesis and browning in white adipose tissue (WAT), which indicates that PNS fail to reduce obesity in leptin gene-deficient mice. The PNS-induced modulation of the gut microbiota exerted a minimal effect on DIO mice with antibiotic-induced microbiome depletion, which confirmed the correlation between altered gut microbiota and the remodeling of adipose tissues in DIO mice. The direct influence of leptin on browning via the AMPKα/STAT3 signaling pathway in C3H101/2 cells supported our in vivo results that signalling through the leptin-AMPK/STAT3 pathway induced by the PNS-modulated gut microbiota was involved in beige adipocyte reconstruction.
Conclusion: Our results revealed that leptin signaling is critical for alterations in microbiota-fat crosstalk and provide promising avenues for therapeutic intervention in the treatment of obesity.

First Authors:
Yu Xu

Correspondence Authors:
Yibin Feng

All Authors:
Yu Xu,Ning Wang,Hor-Yue Tan,Sha Li,Cheng Zhang,Zhangjin Zhang,Yibin Feng

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