Genistein inhibits differentiation of primary human adipocytes

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...

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Published inThe Journal of nutritional biochemistry Vol. 20; no. 2; pp. 140 - 148
Main Authors Park, Hea Jin, Della-Fera, Mary Anne, Hausman, Dorothy B., Rayalam, Srujana, Ambati, Suresh, Baile, Clifton A.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.02.2009
New York, NY: Elsevier Science
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Abstract 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% ( P<.0001) and 50.68±1.34% ( P<.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 down-regulation of ERα and ERβ expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.
AbstractList 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% ( P<.0001) and 50.68±1.34% ( P<.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 down-regulation of ERα and ERβ expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.
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% (P<.0001) and 50.68±1.34% (P<.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 down-regulation of ERα and ERβ expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.
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 beta. In this study, we determined the effect of genistein on adipogenesis and estrogen receptor (ER) alpha and beta expression during differentiation in primary human preadipocytes. Genistein inhibited lipid accumulation in a dose-dependent manner at concentrations of 6.25 microM and higher, with 50 microM genistein inhibiting lipid accumulation almost completely. Low concentrations of genistein (3.25 microM) increased cell viability and higher concentrations (25 and 50 microM) decreased it by 16.48+/-1.35% (P&lt;.0001) and 50.68+/-1.34% (P&lt;.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 gamma, CCAAT/enhancer binding protein alpha, 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 down-regulation of ERalpha and ERbeta expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.
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 beta. In this study, we determined the effect of genistein on adipogenesis and estrogen receptor (ER) alpha and beta expression during differentiation in primary human preadipocytes. Genistein inhibited lipid accumulation in a dose-dependent manner at concentrations of 6.25 microM and higher, with 50 microM genistein inhibiting lipid accumulation almost completely. Low concentrations of genistein (3.25 microM) increased cell viability and higher concentrations (25 and 50 microM) decreased it by 16.48+/-1.35% (P<.0001) and 50.68+/-1.34% (P<.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 gamma, CCAAT/enhancer binding protein alpha, 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 down-regulation of ERalpha and ERbeta expression. This study adds to the elucidation of the molecular pathways involved in the inhibition of adipogenesis by phytoestrogens.
Author Baile, Clifton A.
Park, Hea Jin
Hausman, Dorothy B.
Ambati, Suresh
Della-Fera, Mary Anne
Rayalam, Srujana
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Issue 2
Keywords Phytoestrogen
Estrogen receptor
GPDH activity
Gene expression
Adipogenesis
Human
Isoflavone
Adipocyte
Genistein
Vertebrata
Mammalia
Differentiation
Hormonal receptor
Language English
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Snippet Genistein, a major soy isoflavone, has been reported to exhibit antiadipogenic and proapoptotic potential in vivo and in vitro. It is also a phytoestrogen...
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SubjectTerms adipocytes
Adipocytes - cytology
Adipocytes - drug effects
Adipocytes - enzymology
Adipogenesis
adipose tissue
Biological and medical sciences
cell culture
Cell Differentiation - drug effects
cell proliferation
Cell Survival - drug effects
Cryopreservation
DNA Probes
Estrogen receptor
fatty acid-binding proteins
fatty-acid synthase
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Gene expression
gene expression regulation
genistein
Genistein - pharmacology
glycerol-3-phosphate dehydrogenase (NAD)
Glycerolphosphate Dehydrogenase - metabolism
GPDH activity
hormone receptors
hormone-sensitive lipase
Humans
Kinetics
leptin
lipogenesis
lipoprotein lipase
nutrition-genotype interaction
obesity
perilipin
peroxisomes
Phytoestrogen
plant estrogens
PPAR gamma - genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA - drug effects
RNA - genetics
RNA, Ribosomal, 18S - drug effects
RNA, Ribosomal, 18S - genetics
soy protein
soybean products
sterol regulatory element-binding protein 1
Vertebrates: anatomy and physiology, studies on body, several organs or systems
weight control
weight loss
Title Genistein inhibits differentiation of primary human adipocytes
URI https://dx.doi.org/10.1016/j.jnutbio.2008.01.006
https://www.ncbi.nlm.nih.gov/pubmed/18547799
https://search.proquest.com/docview/66800146
Volume 20
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