Lee Jin-Bong, Yoon Sung-Jin, Lee Sang-Hyun, Lee Moo-Seung, Jung Haiyoung, Kim Tae-Don, Yoon Suk Ran, Choi Inpyo, Kim Ik-Soo, Chung Su Wol, Lee Hee Gu, Min Jeong-Ki, Park Young-Jun
Metabolic Regulation Research CenterKorea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon Republic of Korea.
Department of Functional GenomicsUniversity of Science and Technology, Daejeon, Republic of Korea.
J Endocrinol. 2017 Dec;235(3):223-235. doi: 10.1530/JOE-17-0233.
Healthy expansion of adipose tissue maintains metabolic homeostasis by storing excess chemical energy in increased fat mass. The STAT5-PPAR gamma pathway reportedly regulates adipocyte differentiation, lipid metabolism and adipogenesis. Ginsenoside Rg3 is one of the diverse groups of steroidal saponins, the major active components of ginseng, which have demonstrated pharmacological properties. In this study, we evaluated the therapeutic effects of ginsenoside Rg3 under pathological conditions and We examined the effects of ginsenoside Rg3 on glucose level, insulin sensitivity and lipogenesis in high-fat diet-fed C57BL/6 mice. Ginsenoside Rg3 was also applied to the pre-adipocyte cell line 3T3-L1 to assess the impact on lipogenesis. Ginsenoside Rg3 reduced epididymal white adipose tissue (eWAT) size and hepatic steatosis, and the amount of triglycerides (TGs) in both eWAT and liver. Similar to the murine model, Rg3-treated 3T3-L1 cells showed a reduction in lipid accumulation and amount of total TGs. Ginsenoside Rg3 regulates the expression of PPAR gamma though STAT5 and According to our results, lipid metabolism-related genes were downregulated in the high-fat mice and 3T3-L1 cell line. Rg3 shows potential for the amelioration of obesity-induced pathology, acting though STAT5-PPAR gamma to facilitate the healthy functioning of adipose tissue. This is the first report of evidence that obesity-induced insulin resistance and lipotoxicity can be treated with ginsenoside Rg3, which acts though the STAT5-PPAR gamma pathway and .
脂肪组织的健康扩张通过将多余的化学能量储存为增加的脂肪量来维持代谢稳态。据报道,STAT5-PPARγ途径调节脂肪细胞分化、脂质代谢和脂肪生成。人参皂苷Rg3是甾体皂苷的不同类别之一,是人参的主要活性成分,已显示出药理特性。在本研究中,我们评估了人参皂苷Rg3在病理条件下的治疗效果,并研究了人参皂苷Rg3对高脂饮食喂养的C57BL/6小鼠血糖水平、胰岛素敏感性和脂肪生成的影响。人参皂苷Rg3还应用于前脂肪细胞系3T3-L1,以评估其对脂肪生成的影响。人参皂苷Rg3减少了附睾白色脂肪组织(eWAT)的大小和肝脏脂肪变性,以及eWAT和肝脏中甘油三酯(TGs)的含量。与小鼠模型相似,用Rg3处理的3T3-L1细胞显示脂质积累和总TGs含量减少。人参皂苷Rg3通过STAT5调节PPARγ的表达,根据我们的结果,高脂小鼠和3T3-L1细胞系中与脂质代谢相关的基因被下调。Rg3显示出改善肥胖诱导的病理状况的潜力,通过STAT5-PPARγ途径促进脂肪组织的健康功能。这是第一份有证据表明肥胖诱导的胰岛素抵抗和脂毒性可以用人参皂苷Rg3治疗的报告,人参皂苷Rg3通过STAT5-PPARγ途径发挥作用。