Genistein suppresses adipogenesis of 3T3‐L1 cells via multiple signal pathways

Zhang, Meng; Ikeda, Katsumi; Xu, Jin-Wen; Yamori, Yukio; Gao, Xiumei; Zhang, Boli

doi:10.1002/ptr.2724

Cited by 72 publications

(58 citation statements)

References 29 publications

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“…The activation and phosphorylation of the Akt, P38 and ERK1/2 signaling pathways play a key role in the earliest phases of differentiation (22,23). Akt signaling is indispensable for the regulation of preadipocyte and adipocyte number.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide 1 regulates adipogenesis in 3T3-L1 preadipocytes

Yang

Ren

Song

et al. 2013

International Journal of Molecular Medicine

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Abstract. Glucagon-like peptide 1 (GLP-1), a gut-derived peptide, has been reported to have profound effects on metabolism and to reduce insulin resistance. Adipocyte hyperplasia stimulated by preadipocyte differentiation has a positive effect on adipose tissue insulin sensitivity. However, it remains less clear whether GLP-1 plays a role in adipogenesis. In this study, we examined the effect of GLP-1 on preadipocyte differentiation and investigated the mechanisms that may be involved in this effect. In our 3T3-L1 cell study, we tested the levels of adipocyte-specific markers and signaling pathways during preadipocyte differentiation. In addition, Oil Red O staining was used to examine lipid accumulation. Image Pro Plus 5.02 was used to analyze the size and number of lipid droplets. We found that GLP-1 elevated the protein expression levels of free fatty acid-binding protein 4 (aP2) and the transcription factor peroxisome proliferator-activated receptor-γ (PPAR-γ) in a dose-dependent manner during 3T3-L1 preadipocyte differentiation. Furthermore, RT-PCR results showed that GLP-1 promoted CCAAT/enhancer-binding protein α (C/EBPα) and lipoprotein lipase (LPL) expression at the transcriptional level. These data suggest that GLP-1 promotes preadipocyte differentiation. Our study also found that treatment of the cells with 100 nM GLP-1 enhanced the phosphorylation of Akt signaling during the first 24 h of differentiation. Although Oil Red O staining showed that GLP-1 had no significant effect on lipid accumulation, there were increased numbers of small adipocytes in the cells treated with 100 nM GLP-1. Taken together, these results indicate that GLP-1 regulates 3T3-L1 adipogenesis and the Akt signaling pathway may be involved in this process. The differentiated small adipocytes may have a positive effect against insulin resistance and obesity. IntroductionThe growing prevalence of obesity constitutes a major health problem worldwide (1). Obesity, particularly abdominal obesity, has a strong relationship with insulin resistance and is a major risk factor for type 2 diabetes and cardiovascular disease (2,3). The imbalance between energy intake and expenditure contributes to the development of obesity (1,4); the cellular mechanisms for which include the expansion of white adipose tissue via the hypertrophy of preexisting adipocytes and hyperplasia resulting from the adipogenesis of preadipocytes (4,5). When animals are maintained on a highfat diet, adipo cyte cell size initially increases, followed by an increase in fat cell number upon prolonged over-nutrition (6). In adults, ~10% of fat cells are renewed from preadipocytes annually (7). One study in adults demonstrated that short-term overfeeding increases the adipocyte cell numbers (8). Thus, adipogenesis probably has a role in the pathology of obesity in human adults. However, there are significant differences in lipid and glucose metabolism between adipocyte hypertrophy and hyperplasia (9-11). Recent studies have shown that adipocyte hypertrophy is negatively corre...

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Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide 1 regulates adipogenesis in 3T3-L1 preadipocytes

Yang

Ren

Song

et al. 2013

International Journal of Molecular Medicine

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“…Cells were cultured in a humidifi ed atmosphere at 37°C and 5% CO 2 in DMEM containing conjugated linolenic acid, docosahexanoic acid, epigallocatechin gallate (EGCG), quercetin, resveratrol, and ajoene affect adipogenic differentiation at various life cycle stages of adipocytes (4)(5)(6)(7)(8)(9)(10). These effects are exerted either by induction of apoptosis, inhibition of adipogenesis, stimulating lipolysis, or combinations thereof ( 11 ).…”

Section: Differentiation Of 3t3-l1 and C3h10t1/2 Adipocytesmentioning

confidence: 99%

Rohitukine inhibits in vitro adipogenesis arresting mitotic clonal expansion and improves dyslipidemia in vivo

Varshney

Shankar

Beg

et al. 2014

Journal of Lipid Research

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“…또한, genistein은 마우스3T3-L1 전지방 세포에서 지방세포의 증식 과 지질축적을 억제하며 지방세포의 지방분해를 증가시킨다 는 연구결과들이 보고된 바 있다 [5][6][7]. 게다가, genistein은 여 러 가지 신호 전달과정을 통해 adipogenesis 과정을 저해할 수 있다고 보고 되었다 [19]. 그러나 (Fig.…”

Section: 서 론unclassified

Effects of Genistein on Cell Proliferation and Adipogenesis in Mouse 3T3-L1 Preadipocytes

Lim¹,

Kim²,

Kim³

et al. 2012

Journal of Life Science

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The effects of genistein on cell proliferation and adipogenesis were examined in mouse 3T3-L1 preadipocyte cells. Genistein decreased viability of 3T3-L1 pre-adipocytes in a dose-dependent manner. Oil Red O staining of these cells also indicated that adipogenesis was inhibited by 50 μM genistein treatment. We investigated the molecular mechanisms involved in the decrease in cell viability in genistein-treated 3T3-L1 cells by conducting an oligo DNA microarray analysis. We selected the sirtuin-1 gene, one of the upregulated genes, for further experimentation because sirtuin-1 belongs to the sirtuin family, which is associated with anti-obesity and anti-inflammation activities. We found that four phytochemicals (resveratrol, capsaicin, daidzein, and genistein) could increase sirtuin-1 expression. Genistein was the strongest inducer of sirtuin-1 among the tested phytochemicals. The inhibition of adipogenesis by genistein was recovered by surtuin-1 siRNA transfection. Overall, these results may further our understanding of the molecular mechanisms underlying the inhibition of proliferation and adipogenesis by genistein in mouse 3T3-L1 cells.

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Genistein suppresses adipogenesis of 3T3‐L1 cells via multiple signal pathways

Cited by 72 publications

References 29 publications

Glucagon-like peptide 1 regulates adipogenesis in 3T3-L1 preadipocytes

Glucagon-like peptide 1 regulates adipogenesis in 3T3-L1 preadipocytes

Rohitukine inhibits in vitro adipogenesis arresting mitotic clonal expansion and improves dyslipidemia in vivo

Effects of Genistein on Cell Proliferation and Adipogenesis in Mouse 3T3-L1 Preadipocytes

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