Antiobesity Effects of Ginsenoside Rg1 on 3T3-L1 Preadipocytes and High Fat Diet-Induced Obese Mice Mediated by AMPK

Abstract

Ginsenosides Rg1 is one of the major pharmacologically active saponins in ginseng, which as an antioxidant reduces oxidative damage in the liver and can also be used to prevent cardiovascular diseases and diabetes. However, there is no research targeting the effect of lipid metabolism in high-fat diet (HFD)-induced mice. In this study, we evaluated the anti-obesity effects of Rg1 in 3T3-L1 adipocyte cells and HFD-induced obese C57BL/6J mice. Administration of Rg1 to HFD-induced obese mice significantly decreased body weight, total cholesterol, and total triglyceride levels. In addition to effects in 3T3-L1 cells, Rg1 reduced the accumulation of lipid droplets in a dose-dependent manner. Furthermore, Rg1 exhibits an anti-adipogenic effect via regulation of the expression of the transcriptional factors and lipid metabolism-related genes in vivo and in vitro. We observed that Rg1 administration significantly increased the phosphorylation level of AMP-activated protein kinase (AMPK) in both epididymal white adipose tissue and 3T3-L1 cells. These results indicated that Rg1 works both in an anti-adipogenic and anti-obesity manner through inducing AMPK activation, inhibiting lipogenesis, and decreasing intracellular lipid content, adipocyte size, and adipose weight.

Kisspeptin-10 Promoting the Synthesis of Milk Fat by Inhibiting the AMPK/SIRT6 Signaling Pathway via the GPR54 in Bovine Mammary Epithelial Cells

“…Vitamin D relieves fat deposition in C2C12 cells through AMPK/SIRT1 [29]. Ginsenosides Rg1 reduces fat deposition in adipose tissue and 3T3-L1 cells by activating AMPK [34]. Aged Oolong Tea reduces fat deposits caused by a high-fat diet by activating AMPK [35].…”

A preliminary study on the differential expression of long noncoding RNAs and messenger RNAs in obese and control mice

“…[41][42][43] Oxidative phosphorylation refers to the production of excessive oxygen-free radicals resulting in oxygen-free radicals and related metabolism by the excessive aggregation of products in the mitochondria. [44][45][46] Due to the overproduction of ROS or the imbalance in the antioxidant system, the cells could be damaged, especially the biological macromolecules, such as lipids, proteins, and nucleic acids. These cells would attract more macrophages and then cause the release of proinflammatory cytokines, which would conversely aggravate oxidative stress and eventually lead to obesity.…”

Vanadium-protein complex inhibits human adipocyte differentiation through the activation of β-catenin and LKB1/AMPK signaling pathway

“…Adipocytes are highly specialized cells and can be generated from inducing preadipocytes in the involvement of a series of adipogenic transcription factors and enzymes [8]. It has been demonstrated that several adipogenic transcription factors including PPARγ, C/EBP family (C/EBPα, β, γ), and SREBP-1c can induce adipocyte differentiation (adipogenesis) [7]. Among them, PPARγ, considered as a master regulator for adipocyte differentiation, mainly expressed in adipose tissue and is both necessary and sufficient for adipocyte differentiation [9,10].…”

“…The roles of C/EBP family members in adipogenesis were also interrupted. The activation of C/EBPα was found to be beneficial for enhancing insulin sensitivity in adipocytes [9], and the activation of C/EBPβ and C/EBPγ can stimulate the expression of PPARγ and C/EBPα [8,11], which can further regulate the expression of SREBP-1c and downstream adipocyte-specific proteins involved in lipolysis [7].…”

“…Whereafter these transcription factors can regulate the expression of lipogenic genes including acetyl-CoA carboxylase (ACC), FAS and fatty acid-binding protein 4 (FABP4). These would lead to inhibition of adipocyte differentiation and further antiobesity [7,14]. Therefore, the inhibition of adipocyte differentiation was regarded as a rational treatment strategy for obesity.…”