Effect of some phytoestrogens on metabolism of rat adipocytes

Kandulska, Katarzyna; Nogowski, Leszek; Szkudelski, Tomasz

doi:10.1051/rnd:19990408

Cited by 41 publications

(29 citation statements)

References 14 publications

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“…Genistein has been shown to have potential anti-obesity effects, decreasing food intake, body weight and fat pad weight and inducing adipose tissue apoptosis in vivo [6,7] and inhibiting lipid accumulation and increasing lipolysis in vitro [8][9][10][11]. In this study, we examined the effect of genistein on differentiation, expression of adipocytespecific genes and expression of ERα and ERβ in primary human preadipocyte culture.…”

Section: Discussionmentioning

confidence: 99%

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Genistein inhibits differentiation of primary human adipocytes

Park

Della‐Fera

Hausman

et al. 2009

The Journal of Nutritional Biochemistry

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Genistein, a major soy isoflavone, has been reported to exhibit antiadipogenic and proapoptotic potential in vivo and in vitro. It is also a phytoestrogen which has high affinity to estrogen receptor β. In this study, we determined the effect of genistein on adipogenesis and estrogen receptor (ER) α and β expression during differentiation in primary human preadipocytes. Genistein inhibited lipid accumulation in a dose-dependent manner at concentrations of 6.25 μM and higher, with 50 μM genistein inhibiting lipid accumulation almost completely. Low concentrations of genistein (3.25 μM) increased cell viability and higher concentrations (25 and 50 μM) decreased it by 16.48±1.35% (Pb.0001) and 50.68±1.34% (Pb.0001). Oil Red O staining was used to confirm the effects on lipid accumulation. The inhibition of lipid accumulation was associated with inhibition of glycerol-3-phosphate dehydrogenase activity and down-regulation of expression of adipocyte-specific genes, including peroxisome proliferator-activated receptor γ, CCAAT/enhancer binding protein α, glycerol-3-phosphate dehydrogenase, adipocyte fatty acid binding protein, fatty acid synthase, sterol regulatory element-binding protein 1, perilipin, leptin, lipoprotein lipase and hormone-sensitive lipase. These effects of genistein during the differentiation period were associated with downregulation of ERα and ERβ expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.

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Section: Discussionmentioning

confidence: 99%

“…It has been shown to decrease food intake, body weight and fat pad weight in ovariectomized female mice [6,7]. Genistein has been shown to inhibit lipid accumulation in 3T3-L1 cells [8][9][10] and also to inhibit cell proliferation and increase lipolysis in 3T3-L1 cells and rat adipocytes [8,11].…”

Section: Introductionmentioning

confidence: 99%

Genistein inhibits differentiation of primary human adipocytes

Park

Della‐Fera

Hausman

et al. 2009

The Journal of Nutritional Biochemistry

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“…Recently, some studies reported that genistein blocks adipogenesis and increases lipolysis in 3T3-L1 adipocytes (Harmon et al, 2002;Harmon and Harp, 2001;Hwang et al, 2005) and rat adipocytes (Kandulska et al, 1999;Szkudelska et al, 2000). Genistein produced a suppression effect on adipocyte differentiation by inhibiting the tyrosine phosphorylation of CCAAT/enhancer binding protein beta (C/EBPβ) (Harmon et al, 2002), inducing the expression of peroxisome proliterator-activated receptor alpha (PPARα) (Kim et al, 2004) and activating AMPactivated protein kinase (Hwang et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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

Zhang

Ikeda

et al. 2008

Phytotherapy Research

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Genistein, an isoflavone, was shown to have therapeutic effects for obesity, diabetes and cardiovascular diseases. This study investigated the effect and underlying mechanism of genistein on adipogenesis in 3T3-L1 preadipocytes. Genistein inhibited lipid accumulation and decreased the nonesterified fatty acid (NEFA) content of 3T3-L1 on day 6 after the induction of differentiation with methylisobutylxanthine, dexamethasone and insulin (MDI). Genistein recovered nitric oxide (NO) release suppressed by MDI and the results were consistent with the expression of endothelial NO synthase (eNOS) assayed by western blotting. Pretreatment with genistein inhibited the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) stimulated with 10 microg/mL of insulin. Furthermore, genistein inhibited the expression of fatty acid synthase (FAS) from 178% of the MDI group to 74%. SB203580, a p38 inhibitor, mimicked the FAS inhibition effect of genistein, suggesting that the inhibitory effect of genistein on FAS was partially via the p38 pathway. On the other hand, genistein abolished the phosphorylation of janus-activated kinase 2 (JAK2) in response to MDI. AG490, a JAK2 inhibitor, suppressed the expression of CCAAT/enhancer binding protein alpha (C/EBPalpha), a marker of adipocyte differentiation. The findings suggest that genistein attenuates the differentiation of 3T3-L1 involving multiple signal pathways.

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“…Genistein (G), 5 a soy isoflavone, was shown to decrease food intake, body weight, and fat pad weight in ovariectomized female mice (5,6). In adipocytes, G was shown to inhibit cell proliferation and increase lipolysis (7). In addition to estrogenic effects, G has effects on protein tyrosine kinases, apoptosis, cell proliferation, and angiogenesis (8)(9)(10) and can potentially affect adipose tissue through these mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Potentiates Genistein’s Antiadipogenic and Proapoptotic Effects in 3T3-L1 Adipocytes ,

Rayalam

Della‐Fera

Yang

et al. 2007

The Journal of Nutrition

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Genistein (G) and resveratrol (R) individually inhibit adipogenesis in 3T3-L1 adipocytes and induce apoptosis in cancer cells.We investigated whether the combination of G and R resulted in enhanced effects on adipogenesis, lipolysis, and apoptosis in 3T3-L1 cells. Preadipocytes and mature adipocytes were treated with G and R individually at 50 and 100 mmol/L (G100; R100) and in combination. Both in preadipocytes and mature adipocytes, G and R individually decreased cell viability dose-dependently, but G100 1 R100 further decreased viability by 59 6 0.97% (P , 0.001) and 69.7 6 1.2% (P , 0.001) after 48 h compared with G100 and R100, respectively. G100 1 R100 induced apoptosis 242 6 8.7% (P , 0.001) more than the control after 48 h, whereas G100 and R100 individually increased apoptosis only 46 6 9.2 and 46 6 7.9%, respectively. G and R did not modulate mitogen-activated protein kinase expression by themselves, but G100 1 R100 increased Jun-N-terminal kinase phosphorylation by 38.8 6 4.4% (P , 0.001) and decreased extracellular signal-regulating kinase phosphorylation by 48 6 3.4% (P , 0.001). Individually, G and R at 25 mmol/L (G25; R25) decreased lipid accumulation by 30 6 1.7% and 20.07 6 4.27%, respectively (P , 0.001). However, G25 1 R25 decreased lipid accumulation by 77.9 6 3.4% (P , 0.001). Lipolysis assay revealed that neither G25 nor R25 induced lipolysis, whereas G25 1 R25 significantly increased lipolysis by 25.5 6 4.6%. The adipocyte-specific proteins PPARg and CCAAT/enhancer binding protein-alpha were downregulated after treatment with G 1 R, but no effect was observed with individual compounds. These results indicate that G and R in combination produce enhanced effects on inhibiting adipogenesis, inducing apoptosis, and promoting lipolysis in 3T3-L1 adipocytes. Thus, the combination of G and R is more potent in exerting antiobesity effects than the individual compounds.

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Effect of some phytoestrogens on metabolism of rat adipocytes

Cited by 41 publications

References 14 publications

Genistein inhibits differentiation of primary human adipocytes

Genistein inhibits differentiation of primary human adipocytes

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

Resveratrol Potentiates Genistein’s Antiadipogenic and Proapoptotic Effects in 3T3-L1 Adipocytes ,

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