Rare ginsenosides transformed from stems and leaves of Panax ginseng reverse obesity by promoting browning of white fat through PKA/CREB pathway via REGγ negative regulation

文献类型： 外文期刊

第一作者： Chen, Jianbo

作者： Chen, Jianbo;Sha, Jiyue;Huo, Xiaohui;Li, Zhiman;Qu, Di;Li, Xueqing;Li, Meijia

作者机构：

关键词： Rare ginsenosides; Amino acids; Adipose browning; PKA/CREB signaling pathway; Obesity

期刊名称：JOURNAL OF GINSENG RESEARCH （ 影响因子：5.6； 五年影响因子：5.6 ）

ISSN： 1226-8453

年卷期： 2025 年 49 卷 2 期

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收录情况： SCI

摘要： Background: White adipose tissue (WAT) browning can promote thermogenesis and could be a promising target for treating obesity. Rare ginsenosides transformed from stems and leaves of Panax ginseng (T-GSSL) exhibit numerous biological activities. However, its potential anti-obesity effects and underlying mechanism remain largely unknown. Methods: Five amino acids were selected as the catalysts for the transformation of ginsenosides into rare ginsenosides. An obese mouse model was established by feeding mice a high-fat diet (HFD) for 14 weeks. The effects of T-GSSL on obese mice were assessed by measuring body weight, fat mass, energy expenditure (EE), and glucose tolerance. The 3T3-L1 cells were differentiated into mature adipocytes and incubated with T-GSSL. Immunohistochemistry, co-immunoprecipitation (Co-IP), enzyme-linked immunosorbent assays (ELISA), western blotting (WB), real-time polymerase chain reaction (PCR), and other methods were used to investigate the targets and mechanisms of action of T-GSSL. Results: Ginsenosides in GSSL were hydrolyzed using glutamic acid as a catalyst and 12 rare ginsenosides were produced, with a total conversion rate of 95 %. T-GSSL ameliorated metabolic disorders, lipid ectopic deposition, and obesity, and maintained glucose homeostasis in obese mice. T-GSSL treatment promoted adipose browning and enhanced EE in both HFD mice and 3T3-L1 cells. These effects were decreased in cells treated with a protein kinase A (PKA) antagonist or subjected to PKAc alpha knockdown, whereas they were increased in REG gamma- /- mice. The inhibition of REG gamma alongside the activation of the PKA/CREB pathway elucidates the mechanism through which T-GSSL reverses obesity by promoting the browning of adipose tissue. Conclusions: T-GSSL attenuates diet-induced obesity by promoting adipose browning through the inhibition of REG gamma and subsequent activation of the PKA/CREB pathway.

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