Evidence map›Paper›PMID 42663912›Full record

ArticleChinese journal of integrative medicine2026

Gypenosides Induce Preadipocyte Browning via FXR/Rubicon Pathway-Mediated Inhibition of Autophagy.

Yan-Qiu Wang, Chao Chen, You-Kui Shen

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Article in Chinese journal of integrative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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3 authors.

Yan-Qiu WangDepartment of Endocrinology, Hangzhou Traditional Chinese Medicine Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310007, China.
Chao ChenDepartment of Traditional Chinese Medicine, the Second Affiliated Hospital of Wenzhou Medical University, Hangzhou, 325027, China.
You-Kui ShenDepartment of Neurosurgery, Hangzhou Traditional Chinese Medicine Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310007, China. shenyoukui@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo determine whether gypenosides (GPs) induce preadipocyte browning via famesoid X receptor (FXR)/Rubicon-mediated autophagy inhibition and ameliorate obesity-related metabolic disorders in mice.

methodsIn vitro, differentiated 3T3-L1 preadipocytes were treated with 1-6 µ g/mL GPs. Browning markers [uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 α), PR domain containing 16 (Prdm16)], autophagy markers [microtubule-associated protein 1 light chain 3 form II/form I (LC3II/LC3I), Beclin-1, recombinant autophagy related protein 7 (ATG7), p62], and FXR/Rubicon expression were assessed by Western blot and qPCR. FXR knockdown was performed using shRNA lentivirus. Autophagic flux was evaluated using an mRFP-GFP-LC3 tandem reporter. In vivo, high-fat diet-induced obese mice were randomly divided into 5 groups using a random number sequence (n=6 per group): control, model, low- and high-dose GPs (300, 600 mg/kg per day by oral gavage, respectively), and sitagliptin (SIT, 30 mg/kg daily) groups. All treatments were administered daily for 12 weeks. Metabolic parameters, adipocyte histology, and protein expression in inguinal white adipose tissue were then analyzed.

resultsGPs (3-6 µ g/mL) significantly upregulated UCP1, PGC-1α, and Prdm16 protein levels and reduced the LC3II/LC3I ratio compared with the differentiation medium control (all P<0.01). FXR and Rubicon expression were increased by GPs (P<0.01). FXR knockdown abolished these effects (P<0.01). In obese mice, GPs (600 mg/kg) reduced body weight, serum triglycerides, total cholesterol, and fasting blood glucose, decreased adipocyte size, and increased UCP1, PGC-1α, Prdm16, FXR, and Rubicon while decreasing LC3II/LC3I, Beclin-1, and ATG7 compared with the model group (P<0.05).

conclusionGPs activate FXR/Rubicon signal pathway to inhibit autophagy, inducing preadipocyte browning and offering a novel herbal-based anti-metabolic diseases strategy.

Indexed as

autophagyfarnesoid X receptorGynostemma pentaphyllumgypenosidespreadipocyte browninRubicon

Identifiers

PMID42663912

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