Department of Nutrition Science and Food Hygiene, Xiangya School of Public Health, Central South University, 110 Xiangya Road, Changsha 410078, China.
Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, 110 Xiangya Road, Changsha 410078, China.
Nutrients. 2022 Mar 18;14(6):1287. doi: 10.3390/nu14061287.
Liquiritigenin (LQG) is a natural flavonoid from the herb Glycyrrhiza uralensis Fisch that exhibits multiple biological activities. However, its specific role in antiobesity and its related underlying molecular mechanisms remain unknown. The primary purpose of this study is to explore the effects and regulatory mechanisms of LQG on lipid accumulation in 3T3-L1 adipocytes. The results show that LQG significantly reduced triglyceride levels and downregulated the expression of transcription factors such as CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) in 3T3-L1 adipocytes. Additionally, the expression of sterol-regulatory element-binding protein 1c (SREBP1c), acetyl-CoA carboxylase 1 (ACC1), and fatty acid synthase (FASN) involved in lipogenesis was reduced by treatment with LQG. The protein expression levels of light chain 3B (LC3B), autophagy-related protein 7 (ATG7) and p62 were also modulated by LQG, leading to the suppression of autophagy. Further, LQG activated the phosphorylation of the mammalian target of rapamycin (mTOR), the inhibition of which was followed by the restored expression of autophagy-related proteins. Pretreatment with an mTOR inhibitor also reverted the expression of several genes or proteins involved in lipid synthesis. These results suggest that LQG inhibited lipid accumulation via mTOR-mediated autophagy in 3T3-L1 white adipocytes, indicating the role of LQG as a potential natural bioactive component for use in dietary supplements for preventing obesity.
甘草素（LQG）是甘草中的一种天然类黄酮，具有多种生物活性。然而，其在抗肥胖中的具体作用及其相关的潜在分子机制尚不清楚。本研究的主要目的是探讨 LQG 对 3T3-L1 脂肪细胞中脂质积累的影响及其调节机制。结果表明，LQG 可显著降低 3T3-L1 脂肪细胞中甘油三酯水平，并下调转录因子 CCAAT/增强子结合蛋白α（C/EBPα）和过氧化物酶体增殖物激活受体γ（PPARγ）的表达。此外，LQG 处理还降低了参与脂肪生成的固醇调节元件结合蛋白 1c（SREBP1c）、乙酰辅酶 A 羧化酶 1（ACC1）和脂肪酸合酶（FASN）的表达。LQG 还调节了自噬相关蛋白 7（ATG7）和 p62 的轻链 3B（LC3B）的蛋白表达水平，导致自噬受到抑制。进一步研究表明，LQG 激活了哺乳动物雷帕霉素靶蛋白（mTOR）的磷酸化，抑制 mTOR 后恢复了自噬相关蛋白的表达。mTOR 抑制剂的预处理也使参与脂质合成的几个基因或蛋白的表达恢复正常。这些结果表明，LQG 通过 mTOR 介导的自噬抑制了 3T3-L1 白色脂肪细胞中的脂质积累，表明 LQG 作为一种潜在的天然生物活性成分，可用于预防肥胖的膳食补充剂。
