Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Enrichment of Akkermansia muciniphila by red ginseng promotes GDF15 secretion and suppresses obesity in mice.
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Zhuang Tongxi, Wang Xunjiang, Zheng Wei, Lu Wanyi, Hao Longlong, Wang Xu, Huang Chaokang, Wang Rufeng, Hu Yiren, Wang Zhengtao, Chen Kaixian, Li Tingzhao, Yang Qiaoling, Yang Li, Ding Lili
Аннотация
BACKGROUND: Obesity is a growing global health burden with rising incidence. Red ginseng (RGS), a traditional processed ginseng product, shows potential for improving metabolic parameters, though its anti-obesity mechanism remains incompletely understood.
PURPOSE: This study investigated the therapeutic effects of short-term RGS administration on obesity and sought to elucidate the underlying mechanism.
METHODS: A high-fat diet (HFD)-induced obese mouse model was used to assess short-term RGS effects. Antibiotic treatment and fecal microbiota transplantation were performed to evaluate gut microbiota involvement. 16S rRNA sequencing and metagenomic analysis identified key bacterial species, and mass spectrometry-based proteomics identified A. muciniphila-derived proteins. The growth differentiation factor 15 (GDF15)-GFRAL axis was interrogated using Gfral‒/‒ mice.
RESULTS: Short-term RGS treatment suppressed appetite, reduced body weight, and elevated circulating GDF15 in diet-induced obese (DIO) mice. RGS enriched A. muciniphila, and its depletion abrogated RGS-mediated weight loss and appetite suppression. The A. muciniphila-derived protein Amuc_1631 was identified as a key effector promoting GDF15 secretion. Mechanistically, RGS upregulated colonic Gdf15 transcription via the PERK-eIF2α-ATF4-CHOP axis and activated the brainstem GDF15-GFRAL pathway. The RGS 50% ethanol eluate (RGS/50) fraction was identified as the potential active component responsible for A. muciniphila enrichment and GDF15 elevation.
CONCLUSIONS: This study identifies a gut microbiota-dependent mechanism underlying the anti-obesity effects of RGS, centered on A. muciniphila enrichment and its derived protein Amuc_1631, which promotes GDF15 secretion to suppress food intake via the GDF15-GFRAL axis.
PURPOSE: This study investigated the therapeutic effects of short-term RGS administration on obesity and sought to elucidate the underlying mechanism.
METHODS: A high-fat diet (HFD)-induced obese mouse model was used to assess short-term RGS effects. Antibiotic treatment and fecal microbiota transplantation were performed to evaluate gut microbiota involvement. 16S rRNA sequencing and metagenomic analysis identified key bacterial species, and mass spectrometry-based proteomics identified A. muciniphila-derived proteins. The growth differentiation factor 15 (GDF15)-GFRAL axis was interrogated using Gfral‒/‒ mice.
RESULTS: Short-term RGS treatment suppressed appetite, reduced body weight, and elevated circulating GDF15 in diet-induced obese (DIO) mice. RGS enriched A. muciniphila, and its depletion abrogated RGS-mediated weight loss and appetite suppression. The A. muciniphila-derived protein Amuc_1631 was identified as a key effector promoting GDF15 secretion. Mechanistically, RGS upregulated colonic Gdf15 transcription via the PERK-eIF2α-ATF4-CHOP axis and activated the brainstem GDF15-GFRAL pathway. The RGS 50% ethanol eluate (RGS/50) fraction was identified as the potential active component responsible for A. muciniphila enrichment and GDF15 elevation.
CONCLUSIONS: This study identifies a gut microbiota-dependent mechanism underlying the anti-obesity effects of RGS, centered on A. muciniphila enrichment and its derived protein Amuc_1631, which promotes GDF15 secretion to suppress food intake via the GDF15-GFRAL axis.