Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea.
Department of Public Health, Division of Environmental Health Science, New York Medical College, Valhalla, NY 10595, USA.
Molecules. 2022 Jun 30;27(13):4232. doi: 10.3390/molecules27134232.
We investigated the effects of derhamnosylmaysin (DM) on adipogenesis and lipid accumulation in 3T3-L1 adipocytes. Our data showed that DM inhibited lipid accumulation and adipocyte differentiation in 3T3-L1 cells. Treatment of 3T3-L1 adipocytes with DM decreased the expression of major transcription factors, such as sterol regulatory element-binding protein-1c (SREBP-1c), the CCAAT-enhancer-binding protein (CEBP) family, and peroxisome proliferator-activated receptor gamma (PPARγ), in the regulation of adipocyte differentiation. Moreover, the expression of their downstream target genes related to adipogenesis and lipogenesis, including adipocyte fatty acid-binding protein (aP2), lipoprotein lipase (LPL), stearyl-CoA-desaturase-1 (SCD-1), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS), was also decreased by treatment with DM during adipogenesis. Additionally, DM attenuated insulin-stimulated phosphorylation of Akt. These results first demonstrated that DM inhibited adipogenesis and lipogenesis through downregulation of the key adipogenic transcription factors SREBP-1c, the CEBP family, and PPARγ and inactivation of the major adipogenesis signaling factor Akt, which is intermediated in insulin. These studies demonstrated that DM is a new bioactive compound for antiadipogenic reagents for controlling overweight and obesity.
我们研究了去甲基马桑宁（DM）对 3T3-L1 脂肪细胞成脂作用和脂质积累的影响。我们的数据表明，DM 抑制了 3T3-L1 细胞中的脂质积累和脂肪细胞分化。用 DM 处理 3T3-L1 脂肪细胞降低了主要转录因子的表达，如固醇调节元件结合蛋白-1c（SREBP-1c）、CCAAT 增强子结合蛋白（CEBP）家族和过氧化物酶体增殖物激活受体γ（PPARγ），在调节脂肪细胞分化中。此外，它们与脂肪生成和脂肪生成相关的下游靶基因的表达，包括脂肪细胞脂肪酸结合蛋白（aP2）、脂蛋白脂肪酶（LPL）、硬脂酰辅酶 A 去饱和酶-1（SCD-1）、乙酰辅酶 A 羧化酶（ACC）和脂肪酸合成酶（FAS），在成脂过程中也被 DM 处理所下调。此外，DM 减弱了胰岛素刺激的 Akt 磷酸化。这些结果首次表明，DM 通过下调关键的脂肪生成转录因子 SREBP-1c、CEBP 家族和 PPARγ 以及失活主要的脂肪生成信号因子 Akt（胰岛素中介）来抑制脂肪生成和脂肪生成。这些研究表明，DM 是一种用于控制超重和肥胖的新型抗脂肪生成试剂的生物活性化合物。
