Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, Republic of Korea.
J Nutr Biochem. 2012 Jul;23(7):759-67. doi: 10.1016/j.jnutbio.2011.03.021. Epub 2011 Aug 12.
Licochalcone E (lico E) is a retrochalcone isolated from the root of Glycyrrhiza inflata. Retrochalcone compounds evidence a variety of pharmacological profiles, including anticancer, antiparasitic, antibacterial, antioxidative and superoxide-scavenging properties. In this study, we evaluated the biological effects of lico E on adipocyte differentiation in vitro and obesity-related diabetes in vivo. We employed 3T3-L1 preadipocyte and C3H10T1/2 stem cells for in vitro adipocyte differentiation study and diet-induced diabetic mice for in vivo study. The presence of lico E during adipogenesis induced adipocyte differentiation to a significant degree, particularly at the early induction stage. Licochalcone E evidenced weak, but significant, peroxisome proliferator-activated receptor gamma (PPARγ) ligand-binding activity. Two weeks of lico E treatment lowered blood glucose levels and serum triglyceride levels in the diabetic mice. Additionally, treatment with lico E resulted in marked reductions in adipocyte size and increases in the mRNA expression levels of PPARγ in white adipose tissue (WAT). Licochalcone E was also shown to significantly stimulate Akt signaling in epididymal WAT. In conclusion, lico E increases the levels of PPARγ expression, at least in part, via the stimulation of Akt signals and functions as a PPARγ partial agonist, and this increased PPARγ expression enhances adipocyte differentiation and increases the population of small adipocytes, resulting in improvements in hyperglycemia and hyperlipidemia under diabetic conditions.
甘草查尔酮 E(lico E)是从甘草根中分离得到的一种反式查尔酮。反式查尔酮类化合物具有多种药理作用,包括抗癌、抗寄生虫、抗菌、抗氧化和超氧阴离子清除作用。在这项研究中,我们评估了lico E 在体外脂肪细胞分化和体内肥胖相关糖尿病中的生物学效应。我们使用 3T3-L1 前脂肪细胞和 C3H10T1/2 干细胞进行体外脂肪细胞分化研究,并用饮食诱导的糖尿病小鼠进行体内研究。在脂肪生成过程中存在lico E 可显著诱导脂肪细胞分化,特别是在早期诱导阶段。甘草查尔酮 E 具有较弱但显著的过氧化物酶体增殖物激活受体γ(PPARγ)配体结合活性。2 周的lico E 治疗可降低糖尿病小鼠的血糖和血清甘油三酯水平。此外,lico E 治疗导致白色脂肪组织(WAT)中脂肪细胞大小显著减小和 PPARγ mRNA 表达水平增加。甘草查尔酮 E 还可显著刺激附睾 WAT 中的 Akt 信号。总之,lico E 通过刺激 Akt 信号增加 PPARγ 的表达水平,至少部分是通过刺激 Akt 信号,并且这种增加的 PPARγ 表达增强了脂肪细胞分化,增加了小脂肪细胞的数量,从而改善了糖尿病条件下的高血糖和高血脂。