Abstract
BackgroundObesity, characterized by the excessive accumulation of triglycerides in adipocytes and their decreased excretion from adipocytes, is closely related to various health problems. Ginsenoside Rb1 (Rb1), the most active component of the traditional Chinese medicine ginseng, has been reported to have positive effects on lipid metabolism. The aim of the present study was to determine the protective effects of Rb1 on glycolipid metabolism under obesity conditions and its mechanisms and to reveal the signaling pathways involved.MethodsIn our study, male C57BL/6 mice with obesity induced by a high-fat diet (HFD) and mature 3 T3-L1 adipocytes were used to investigate the role of Rb1 in lipid accumulation and explore its possible molecular mechanism in vivo and in vitro, respectively.ResultsRb1 reduced the body weight, fat mass, adipocytes size and serum free fatty acid (FFA) concentration of obese mice. In differentiated 3 T3-L1 adipocytes, Rb1 reduced the accumulation of lipid droplets and stimulated output of triglycerides. Additionally, the expression of peroxisome proliferator-activated receptor gamma (PPARγ), phosphorylated PPARγ (Ser112) and aquaporin 7 (AQP7) was upregulated in adipocytes and adipose tissues upon Rb1 treatment. However, intervention of GW9662, PPARγ antagonist, attenuated Rb1-mediated effects on glycolipid metabolism and AQP7 levels.ConclusionsThese data indicated that Rb1 reduced body weight and improved glycolipid metabolism by upregulating PPARγ and AQP7 protein levels. Our study indicated a potential role for Rb1 in the prevention and treatment of obesity.
Highlights
Obesity, characterized by the excessive accumulation of triglycerides in adipocytes and their decreased excretion from adipocytes, is closely related to various health problems
Ginsenoside Rb1 (Rb1) reduced body weight and fat mass partially in a Peroxisome Proliferator-activated Receptor Gamma (PPARγ)-dependent manner To confirm the effects of Rb1 on body weight in obese mice, we established a mouse model of obesity through high-fat diet (HFD) feeding
To further determine the role of PPARγ in Rb1-induced body weight and fat mass loss, mice were intraperitoneally injected with GW9662, an antagonist of PPARγ
Summary
Obesity, characterized by the excessive accumulation of triglycerides in adipocytes and their decreased excretion from adipocytes, is closely related to various health problems. Adipose tissue mass is determined by the storage of triglycerides in adipocytes and their removal from adipocytes. High storage but low removal of triglyceride promotes fat tissue accumulation and obesity [4]. This demonstrates that promoting the rate of triglyceride removal from adipocytes is an important antiobesity therapeutic target. AQP7-depleted mice, showed progressive adipocyte hypertrophy, increased fat mass and metabolic disorders [9]. These effects are thought to be relevant to reduced adipocyte glycerol permeability and the subsequent accumulation of intracellular glycerol and triacylglycerol [10]. PPARγ regulates AQP7 expression through binding of the PPARγ-retinoid X receptor complex to the peroxisome proliferator-activated receptor response element (PPRE) region in the AQP7 gene promoter
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