Abstract
Obesity is a major human health problem associated with various diseases, including cardiac injury and type 2 diabetes. Trapa japonica Flerov (TJF) has been used in traditional oriental medicine to treat diabetes. In this study, we evaluated the inhibitory effect of and the mechanism underlying the effect of TJF extract on adipogenesis in 3T3-L1 cells. The effects of TJF extract on cell viability were analyzed using a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, and the anti-adipogenic effect was measured by oil red O staining. The expression of peroxisomal proliferator activated receptor (PPAR)γ, CCAAT/enhancer-binding protein-α (C/EBP)α, adenosine monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), adiponectin, and fatty acid binding protein (FABP)4 involved in adipogenesis was determined by western blot analysis. TJF extract effectively inhibited lipid accumulation and the expression of PPARγ and C/EBPα in 3T3-L1 cells. TJF also increased the phosphorylation of AMPK and ACC, and decreased the expression of adiponectin and FABP4. These results indicate that TJF extract exerts its anti-obesity effect through the downregulation of adipogenic transcription factors and adipogenic marker genes.
Highlights
Obesity is the result of imbalance between energy intake and energy expenditure, and greatly increases the risk of numerous associated diseases, including heart disease, hypertension, stroke, cancer, diabetes, and osteoarthritis [1] [2]
Adipose tissue mass can be regulated by the suppression of adipogenesis, which is the development of mature fat cells from fibroblastic preadipocytes [6]
We examined whether Trapa japonica Flerov (TJF) extract affects adipocyte differentiation, and the expression of adipogenic transcription factors and related proteins in 3T3-L1 cells
Summary
Obesity is the result of imbalance between energy intake and energy expenditure, and greatly increases the risk of numerous associated diseases, including heart disease, hypertension, stroke, cancer, diabetes, and osteoarthritis [1] [2]. Determining the molecular mechanisms regulating adipocytes has crucial implications for the development of therapeutics targeting obesity and obesity-associated diseases. Reducing lipid accumulation through the inhibition of adipocyte differentiation may play a crucial role in preventing obesity. Obesity is known to be associated with excessive growth of adipose tissue mass, through increases in both the number and the size of fat cells [5]. Adipose tissue mass can be regulated by the suppression of adipogenesis, which is the development of mature fat cells from fibroblastic preadipocytes [6]. Adipokines, such as peroxisome proliferator activated receptor (PPAR)γ and CCAAT/enhancer-binding (C/EBP)α, directly regulate the development of fat cells [7]. PPARγ is highly expressed in adipose tissue, where it plays essential roles in adipogenesis [8]
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