Abstract
Although ginsenosides Rb1 and Rg3 have been identified as the significant ginsenosides found in red ginseng that confer anti-diabetic actions, it is unclear whether insulin-sensitizing effects are mediated by the individual compounds or by their combination. To determine the effect of ginsenosides Rb1 and Rg3 on adipocyte differentiation, 3T3-L1 preadipocytes were induced to differentiate the standard hormonal inducers in the absence or presence of ginsenosides Rb1 or Rg3. Additionally, we determined the effects of Rb1, Rg3, or their combination on the expression of genes related to adipocyte differentiation, adipogenic transcription factors, and the insulin signaling pathway in 3T3-L1 cells using semi-quantitative RT-PCR. Rb1 significantly increased the expression of CEBPα, PPARγ, and aP2 mRNAs. However, Rg3 exerted its maximal stimulatory effect on these genes at 1 μM concentration, while a high concentration (50 μM) showed inhibitory effects. Similarly, treatment with Rb1 and Rg3 (1 μM) increased the expression of IRS-1, Akt, PI3K, GLUT4, and adiponectin. Importantly, co-treatment of Rb1 and Rg3 (9:1) induced the maximal expression levels of these mRNAs. Our data indicate that the anti-diabetic activity of red ginseng is, in part, mediated by synergistic actions of Rb1 and Rg3, further supporting the significance of minor Rg3.
Highlights
Enlarged adipocytes and excess adiposity play a key role in the metabolic and cardiovascular complications associated with obesity [1]
This clearly suggests that impaired formation of new adipocytes through preadipocyte differentiation is linked to the pathological expansion of adipose tissue (AT), as evidenced by decreases in insulin sensitivity and expression of mRNAs by differentiation markers such as peroxisome proliferator-activated receptor (PPARγ), glucose transporter 4 (GLUT4), and adiponectin [6,7]
Ginsenosides Rb1 and Rg3 Enhanced the Differentiation of 3T3-L1 Preadipocytes
Summary
Enlarged adipocytes and excess adiposity play a key role in the metabolic and cardiovascular complications associated with obesity [1]. Our current understanding is that hypertrophic obesity is strongly associated with obesity-related insulin resistance and type 2 diabetes (T2D), while hyperplastic obesity is not usually linked to these metabolic consequences, which are seen in 20–30% of obese individuals characterized as “obese but metabolically normal” [2,3,4,5] This clearly suggests that impaired formation of new adipocytes through preadipocyte differentiation (i.e., adipogenesis) is linked to the pathological expansion of adipose tissue (AT), as evidenced by decreases in insulin sensitivity and expression of mRNAs by differentiation markers such as peroxisome proliferator-activated receptor (PPARγ), glucose transporter 4 (GLUT4), and adiponectin [6,7]. Adipocytes have recently been emerging as a therapeutic target for obesity-associated metabolic disorders and introducing agents that promote preadipocyte differentiation and/or lipid oxidation would be a promising strategy for obesity-induced metabolic disorders
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