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Abstract
Soy isoflavones are popular ingredients with anti-adipogenic and anti-lipogenic properties. The anti-adipogenic and anti-lipogenic properties of genistein are well-known, but those of genistin and glycitein remain unknown, and those of daidzein are characterized by contrasting data. Therefore, the purpose of our study was to investigate the effects of daidzein, glycitein, genistein, and genistin on adipogenesis and lipogenesis in 3T3-L1 cells. Proliferation of 3T3-L1 preadipocytes was unaffected by genistin and glycitein, but it was affected by 50 and 100 µM genistein and 100 µM daidzein for 48 h. Among the four isoflavones, only 50 and 100 µM genistin and genistein markedly suppressed lipid accumulation during adipogenesis in 3T3-L1 cells through a similar signaling pathway in a dose-dependent manner. Genistin and genistein suppress adipocyte-specific proteins and genes, such as peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), and adipocyte binding protein 2 (aP2)/fatty acid-binding protein 4 (FABP4), and lipogenic enzymes such as ATP citrate lyase (ACL), acetyl-CoA carboxylase 1 (ACC1), and fatty acid synthase (FAS). Both isoflavones also activate AMP-activated protein kinase α (AMPKα), an essential factor in adipocyte differentiation, and inhibited sterol regulatory element-binding transcription factor 1c (SREBP-1c). These results indicate that genistin is a potent anti-adipogenic and anti-lipogenic agent.
Highlights
Obesity is the status of increased adipose tissue mass and one of the metabolic diseases leading to public health problems worldwide [1]
The toxicity of soy isoflavones was investigated before monitoring the effects on adipocyte differentiation. 3T3-L1 preadipocytes were incubated with 0, 25, 50, or 100 μM daidzein, glycitein, genistein, or genistin for 24 and 48 h, and the cytotoxicity was analyzed using CCK-8 and live/dead cell assays (Figure 1)
After 24 h, 25–100 μM glycitein, genistein, and genistin and 25–50 μM daidzein did not affect the proliferation of 3T3-L1 preadipocytes
Summary
Obesity is the status of increased adipose tissue mass and one of the metabolic diseases leading to public health problems worldwide [1]. Obese people have two internal characteristics: an increase in the fat cell number (hyperplasia) and the adipose cell size (hypertrophy) [2]. Adipogenesis is the process of cell differentiation from preadipocytes into mature adipocytes leading to hyperplasia [3]. Lipogenesis is the process of fatty acid and triglyceride synthesis by the conversion of acetyl-CoA into triglycerides for storage as fat leading to hypertrophy [4]. According to in vitro studies using 3T3-L1 cells, hormones or drugs such as insulin and β-adrenoceptor agonists stimulate fibroblast-like 3T3-L1 cells causing differentiation into adipocyte-like cells and lipid accumulation [5,6,7,8,9]. Incubating 3T3-L1 preadipocytes with the MDI media (a mixture of 3-isobutyl-1-methylxanthine (M), dexamethasone (D), and insulin (I)) promotes a synchronized cell cycle, mitotic clonal expansion (MCE), and adipogenesis [10,11]
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