Sulforaphane Inhibits Mitotic Clonal Expansion During Adipogenesis Through Cell Cycle Arrest
Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenes...
Saved in:
| Published in | Obesity (Silver Spring, Md.) Vol. 20; no. 7; pp. 1365 - 1371 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.07.2012
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1930-7381 1930-739X 1930-739X |
| DOI | 10.1038/oby.2011.388 |
Cover
| Abstract | Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3–L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half‐maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator‐activated receptor γ (PPARγ) and CCAAT/enhancer‐binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early‐stage biomarker of adipogenesis, decreased in a concentration‐dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G0/G1 phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early‐stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G0/G1 phase through upregulation of p27 expression. |
|---|---|
| AbstractList | Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3–L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half‐maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator‐activated receptor γ (PPARγ) and CCAAT/enhancer‐binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early‐stage biomarker of adipogenesis, decreased in a concentration‐dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G
0
/G
1
phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early‐stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G
0
/G
1
phase through upregulation of p27 expression. Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 mol/l). The expression of peroxisome proliferatoractivated receptor (PPAR) and CCAAT/enhancer-binding protein (C/EBP), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBP, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 mol/l). The proliferation of adipocytes treated with 20 mol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G0/G1 phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G0/G1 phase through upregulation of p27 expression.[PUBLICATION ABSTRACT] Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3-L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G(0)/G(1) phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G(0)/G(1) phase through upregulation of p27 expression.Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3-L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G(0)/G(1) phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G(0)/G(1) phase through upregulation of p27 expression. Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3–L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half‐maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator‐activated receptor γ (PPARγ) and CCAAT/enhancer‐binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early‐stage biomarker of adipogenesis, decreased in a concentration‐dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G0/G1 phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early‐stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G0/G1 phase through upregulation of p27 expression. Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3-L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G(0)/G(1) phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G(0)/G(1) phase through upregulation of p27 expression. |
| Author | Yoo, Hwan‐Soo Lee, Youn‐Sun Lee, Yong‐Moon Hong, Jin‐Tae Choi, Kyeong‐Mi Yun, Yeo‐Pyo Sin, Dong‐Mi Lee, Seunghyun Lee, Mi Kyeong |
| Author_xml | – sequence: 1 givenname: Kyeong‐Mi surname: Choi fullname: Choi, Kyeong‐Mi – sequence: 2 givenname: Youn‐Sun surname: Lee fullname: Lee, Youn‐Sun – sequence: 3 givenname: Dong‐Mi surname: Sin fullname: Sin, Dong‐Mi – sequence: 4 givenname: Seunghyun surname: Lee fullname: Lee, Seunghyun – sequence: 5 givenname: Mi Kyeong surname: Lee fullname: Lee, Mi Kyeong – sequence: 6 givenname: Yong‐Moon surname: Lee fullname: Lee, Yong‐Moon – sequence: 7 givenname: Jin‐Tae surname: Hong fullname: Hong, Jin‐Tae – sequence: 8 givenname: Yeo‐Pyo surname: Yun fullname: Yun, Yeo‐Pyo – sequence: 9 givenname: Hwan‐Soo surname: Yoo fullname: Yoo, Hwan‐Soo |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22282047$$D View this record in MEDLINE/PubMed |
| BookMark | eNp90U1PGzEQBmCrAhG-bj1Xlnrh0KT-yK7Xx7BQQAri0CCBVMmyvd7EyLEXe1c0_75GAQ6R6Mk-PDP2zHsE9nzwBoCvGE0wotXPoDYTgjCe0Kr6Ag4xp2jMKH_Y-7hXeASOUnpCaFqiAh-AESGkImjKDsGf34NrQ5TdSnoDb_zKKtsneGv70FsNaxe8dPDybyd9ssHDiyFav4SzxnZhabxJNsHFKoZhuYK1cQ7WG-0MnMVoUn8C9lvpkjl9O4_B_a_LRX09nt9d3dSz-VhPy4KMNacl5wy3TCJStqrVqlSSmwLRkpVMGdowznhRyUI1mjaEM6MriVpFjFGtpMfgbNu3i-F5yA-LtU06_ybPFIYkMCKEMlZRlun3HfoUhphn3CpcIFbirL69qUGtTSO6aNcybsT73jIgW6BjSCmaVmjbyz5vqI_SutxLvIYjcjjiNRyRw8lFP3aK3vt-wvGWv1hnNv-14u78kUwpof8ADsWf6g |
| CitedBy_id | crossref_primary_10_3390_molecules25153346 crossref_primary_10_3390_ijms25020693 crossref_primary_10_1155_2014_415097 crossref_primary_10_17221_8665_CJAS crossref_primary_10_1016_j_jnutbio_2021_108885 crossref_primary_10_3390_molecules24101894 crossref_primary_10_1016_j_bbrc_2012_08_107 crossref_primary_10_1096_fj_201901569R crossref_primary_10_3389_fnut_2020_00111 crossref_primary_10_3390_nu14183814 crossref_primary_10_1016_j_ejmech_2017_10_034 crossref_primary_10_1002_ptr_6089 crossref_primary_10_1055_a_1853_7101 crossref_primary_10_1039_C5FO00397K crossref_primary_10_1155_2018_4159013 crossref_primary_10_1080_09168451_2018_1514247 crossref_primary_10_1194_jlr_M039925 crossref_primary_10_1111_jfbc_13886 crossref_primary_10_1016_j_phymed_2021_153715 crossref_primary_10_1016_j_mam_2012_06_010 crossref_primary_10_1016_j_freeradbiomed_2018_02_004 crossref_primary_10_2147_DMSO_S281186 crossref_primary_10_1371_journal_pone_0150913 crossref_primary_10_1155_2015_407580 crossref_primary_10_1016_j_metabol_2017_01_021 crossref_primary_10_3390_ijms23042299 crossref_primary_10_2217_epi_15_74 crossref_primary_10_3390_foods12050925 crossref_primary_10_3945_an_113_004705 crossref_primary_10_3390_molecules24061157 crossref_primary_10_1016_j_ejphar_2022_174991 crossref_primary_10_1016_j_ejphar_2022_175002 crossref_primary_10_1002_ptr_6434 crossref_primary_10_3390_ijms19061693 crossref_primary_10_7554_eLife_67368 crossref_primary_10_1016_j_jff_2018_02_021 crossref_primary_10_1016_j_taap_2016_07_021 crossref_primary_10_1002_mnfr_201900183 crossref_primary_10_1016_j_mam_2017_01_008 crossref_primary_10_1016_j_jff_2015_10_024 crossref_primary_10_1016_j_vph_2013_06_003 crossref_primary_10_3892_mmr_2017_8235 crossref_primary_10_3390_molecules201219796 crossref_primary_10_1002_jsfa_8898 crossref_primary_10_1371_journal_pone_0132151 crossref_primary_10_1021_acs_jafc_8b04330 crossref_primary_10_3390_nu4121868 crossref_primary_10_1002_jcb_25093 crossref_primary_10_1089_jmf_2021_K_0163 crossref_primary_10_1002_lipd_12123 crossref_primary_10_1007_s12272_013_0251_y crossref_primary_10_1002_ptr_6065 crossref_primary_10_1016_j_jnutbio_2016_01_009 crossref_primary_10_1016_j_nut_2021_111240 crossref_primary_10_1016_j_jnutbio_2022_109238 crossref_primary_10_1016_j_ejmech_2025_117346 crossref_primary_10_1016_j_jnutbio_2013_10_007 crossref_primary_10_1111_jfbc_13528 crossref_primary_10_1016_j_phytol_2017_12_011 crossref_primary_10_1248_bpb_b17_00837 crossref_primary_10_1016_j_jff_2015_09_060 crossref_primary_10_1016_j_jep_2021_114410 crossref_primary_10_1080_09168451_2017_1372181 crossref_primary_10_1002_mnfr_201500021 crossref_primary_10_1016_j_biochi_2014_06_010 crossref_primary_10_1016_j_cbi_2014_12_027 crossref_primary_10_1016_j_phymed_2013_10_009 crossref_primary_10_1038_s41598_021_87367_9 crossref_primary_10_1038_s41598_021_98385_y crossref_primary_10_1002_oby_22145 crossref_primary_10_3390_antiox11101854 crossref_primary_10_3390_nu13103624 crossref_primary_10_3390_molecules27030624 crossref_primary_10_1016_j_bbrc_2015_12_049 crossref_primary_10_1002_ptr_6333 crossref_primary_10_1021_acs_jafc_4c01115 crossref_primary_10_1007_s11101_024_10021_5 crossref_primary_10_1016_j_cbi_2016_07_034 crossref_primary_10_3390_cells11040754 crossref_primary_10_1007_s10068_019_00672_y |
| Cites_doi | 10.1093/carcin/bgg178 10.4161/cc.2.4.427 10.1016/j.bbrc.2010.04.163 10.1006/scdb.1998.0276 10.1002/(SICI)1097-4644(1999)75:32 <59::AID-JCB8>3.0.CO;2-1 10.1210/en.139.4.1638 10.1023/A:1011863414321 10.1016/j.bcp.2005.03.015 10.1002/dmr.5610050804 10.1146/annurev.nu.14.070194.000531 10.1593/tlo.10235 10.1055/s-0030-1270712 10.4161/cc.2.6.550 10.1152/physrev.1998.78.3.783 10.1002/biof.5520220154 10.1016/j.bbrc.2008.04.188 10.1093/eurheartj/ehp317 10.1093/jn/134.5.1134 10.1074/jbc.271.49.31372 10.1248/bpb.33.1610 10.1074/jbc.M000759200 10.1007/s00280-005-0050-3 10.1016/j.bbrc.2008.03.129 10.1128/MCB.22.20.7226-7241.2002 10.1016/j.bbrc.2006.07.095 10.1152/ajpcell.2001.280.6.C1540 10.1167/iovs.04-1120 10.1093/jn/130.12.3122S 10.1073/pnas.0137044100 10.1016/S0021-9258(18)89059-7 10.1007/s00125-009-1588-0 10.1080/10409230591008189 10.1126/science.274.5293.1672 10.1152/ajpcell.00569.2004 10.1074/jbc.M207776200 10.1074/jbc.273.45.29864 10.1016/j.phrs.2009.11.009 10.1210/endo.137.8.8754791 |
| ContentType | Journal Article |
| Copyright | 2012 North American Association for the Study of Obesity (NAASO) Copyright Nature Publishing Group Jul 2012 |
| Copyright_xml | – notice: 2012 North American Association for the Study of Obesity (NAASO) – notice: Copyright Nature Publishing Group Jul 2012 |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM K9. 7X8 |
| DOI | 10.1038/oby.2011.388 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic |
| DatabaseTitleList | CrossRef ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic MEDLINE |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1930-739X |
| EndPage | 1371 |
| ExternalDocumentID | 2696268401 22282047 10_1038_oby_2011_388 OBY2432 |
| Genre | article Research Support, Non-U.S. Gov't Journal Article Feature |
| GroupedDBID | --- 05W 0R~ 123 1OC 29N 2FS 2WC 31~ 33P 39C 3SF 4.4 50Y 52U 52V 53G 70F 8-1 AAESR AAEVG AAFWJ AAHBH AAHQN AAIPD AAMMB AAMNL AANLZ AAONW AASGY AAWTL AAXRX AAYCA AAZKR ABCUV ABIVO ABJNI ABLJU ABQWH ABXGK ACAHQ ACCZN ACGFS ACGOF ACMXC ACPOU ACXBN ACXQS ADBBV ADBTR ADEOM ADIZJ ADKYN ADMGS ADOZA ADXAS ADZMN AEFGJ AEIGN AEIMD AENEX AEUYR AEYWJ AFBPY AFFPM AFGKR AFWVQ AFZJQ AGHNM AGXDD AGYGG AHBTC AHMBA AIACR AIDQK AIDYY AITYG AIURR ALMA_UNASSIGNED_HOLDINGS ALUQN ALVPJ AMBMR AMYDB ATUGU AZVAB BAWUL BFHJK BHBCM BKNYI BMXJE BOGZA BPHCQ BRXPI BVXVI CS3 DCZOG DIK DPXWK DRFUL DRMAN DRSTM DU5 E3Z EBS EJD EMOBN F5P FUBAC G-S GODZA HGLYW HZ~ KBYEO LATKE LEEKS LH4 LITHE LOXES LUTES LW6 LYRES MEWTI MRFUL MRMAN MRSTM MSFUL MSMAN MSSTM MXFUL MXMAN MXSTM MY~ O66 O9- OK1 P2W PQQKQ PROAC R.K ROL SUPJJ WBKPD WHG WHWMO WIH WIJ WIK WIN WOHZO WOQ WQJ WVDHM WXSBR YHZ AAHHS AAYXX ACCFJ AEEZP AEQDE AIWBW AJBDE ALIPV CITATION CGR CUY CVF ECM EIF NPM K9. 7X8 |
| ID | FETCH-LOGICAL-c4652-c9369971f7a026fbfcb6ba9e5036767be3d797958a5bdc3d297ec8a0fb2eebfa3 |
| ISSN | 1930-7381 1930-739X |
| IngestDate | Fri Sep 05 09:00:22 EDT 2025 Fri Jul 25 23:53:49 EDT 2025 Mon Jul 21 05:47:36 EDT 2025 Tue Jul 01 01:16:08 EDT 2025 Thu Apr 24 22:54:33 EDT 2025 Wed Sep 03 09:01:10 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 7 |
| Language | English |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c4652-c9369971f7a026fbfcb6ba9e5036767be3d797958a5bdc3d297ec8a0fb2eebfa3 |
| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://onlinelibrary.wiley.com/doi/pdfdirect/10.1038/oby.2011.388 |
| PMID | 22282047 |
| PQID | 1022150761 |
| PQPubID | 105348 |
| PageCount | 7 |
| ParticipantIDs | proquest_miscellaneous_1022377837 proquest_journals_1022150761 pubmed_primary_22282047 crossref_citationtrail_10_1038_oby_2011_388 crossref_primary_10_1038_oby_2011_388 wiley_primary_10_1038_oby_2011_388_OBY2432 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | July 2012 |
| PublicationDateYYYYMMDD | 2012-07-01 |
| PublicationDate_xml | – month: 07 year: 2012 text: July 2012 |
| PublicationDecade | 2010 |
| PublicationPlace | Oxford, UK |
| PublicationPlace_xml | – name: Oxford, UK – name: United States – name: Silver Spring |
| PublicationTitle | Obesity (Silver Spring, Md.) |
| PublicationTitleAlternate | Obesity (Silver Spring) |
| PublicationYear | 2012 |
| Publisher | Blackwell Publishing Ltd |
| Publisher_xml | – name: Blackwell Publishing Ltd |
| References | 2004; 22 2010; 33 1989; 5 2010; 53 2010; 31 2006; 57 2001; 280 2004; 25 2002; 277 2005; 40 2000; 130 2011; 10 2000; 275 1998; 139 1985; 260 2005; 46 2010; 61 2005; 69 1999 1998; 273 2004; 134 2005; 288 1984; 13 2002; 22 2003; 2 2010; 396 1996; 271 1994; 14 2006; 29 1999; 10 2001; 2 1996; 274 2010; 3 1996; 137 2006; 348 1998; 78 2003; 100 2008; 372 2008; 371 e_1_2_7_5_2 e_1_2_7_3_2 e_1_2_7_2_2 e_1_2_7_9_2 e_1_2_7_8_2 e_1_2_7_7_2 e_1_2_7_6_2 e_1_2_7_18_2 e_1_2_7_17_2 e_1_2_7_16_2 e_1_2_7_15_2 e_1_2_7_14_2 e_1_2_7_40_2 e_1_2_7_13_2 e_1_2_7_41_2 e_1_2_7_12_2 e_1_2_7_11_2 e_1_2_7_10_2 Shan Y (e_1_2_7_19_2) 2006; 29 e_1_2_7_26_2 e_1_2_7_27_2 e_1_2_7_28_2 e_1_2_7_29_2 Martin RJ (e_1_2_7_4_2) 1984; 13 e_1_2_7_25_2 e_1_2_7_24_2 e_1_2_7_30_2 e_1_2_7_23_2 e_1_2_7_31_2 e_1_2_7_22_2 e_1_2_7_32_2 e_1_2_7_21_2 e_1_2_7_33_2 e_1_2_7_20_2 e_1_2_7_34_2 e_1_2_7_35_2 e_1_2_7_36_2 e_1_2_7_37_2 e_1_2_7_38_2 e_1_2_7_39_2 |
| References_xml | – volume: 61 start-page: 342 year: 2010 end-page: 348 article-title: Sulforaphane protects ischemic injury of hearts through antioxidant pathway and mitochondrial K(ATP) channels publication-title: Pharmacol Res – volume: 33 start-page: 1610 year: 2010 end-page: 1614 article-title: Inhibitory effects of coumarins from the stem barks of Fraxinus rhynchophylla on adipocyte differentiation in 3T3‐L1 cells publication-title: Biol Pharm Bull – volume: 46 start-page: 979 year: 2005 end-page: 987 article-title: Sulforaphane induces thioredoxin through the antioxidant‐responsive element and attenuates retinal light damage in mice publication-title: Invest Ophthalmol Vis Sci – volume: 139 start-page: 1638 year: 1998 end-page: 1644 article-title: Modulation of insulin‐like growth factor I mitogenic signaling in 3T3‐L1 preadipocyte differentiation publication-title: Endocrinology – volume: 14 start-page: 99 year: 1994 end-page: 129 article-title: Regulation of adipocyte development publication-title: Annu Rev Nutr – volume: 78 start-page: 783 year: 1998 end-page: 809 article-title: Understanding adipocyte differentiation publication-title: Physiol Rev – volume: 57 start-page: 317 year: 2006 end-page: 327 article-title: p53‐independent G1 cell cycle arrest of human colon carcinoma cells HT‐29 by sulforaphane is associated with induction of p21CIP1 and inhibition of expression of cyclin D1 publication-title: Cancer Chemother Pharmacol – volume: 348 start-page: 571 year: 2006 end-page: 578 article-title: Berberine inhibits 3T3‐L1 adipocyte differentiation through the PPARgamma pathway publication-title: Biochem Biophys Res Commun – volume: 31 start-page: 222 year: 2010 end-page: 226 article-title: Obesity paradox in a cohort of 4880 consecutive patients undergoing percutaneous coronary intervention publication-title: Eur Heart J – volume: 2 start-page: 538 year: 2003 end-page: 544 article-title: A structural analysis of the qualitative networks regulating the cell cycle and apoptosis publication-title: Cell Cycle – volume: 134 start-page: 1134 year: 2004 end-page: 1138 article-title: Breast cancer risk in premenopausal women is inversely associated with consumption of broccoli, a source of isothiocyanates, but is not modified by GST genotype publication-title: J Nutr – volume: 371 start-page: 185 year: 2008 end-page: 190 article-title: Rehmannia inhibits adipocyte differentiation and adipogenesis publication-title: Biochem Biophys Res Commun – volume: 137 start-page: 3590 year: 1996 end-page: 3593 article-title: Expression of a constitutively activated form of protein kinase B (c‐Akt) in 3T3‐L1 preadipose cells causes spontaneous differentiation publication-title: Endocrinology – volume: 10 start-page: 1020 year: 2011 end-page: 1023 article-title: Hydroxyframoside B, a secoiridoid of fraxinus rhynchophylla, inhibits adipocyte differentiation in 3T3‐L1 cells publication-title: Planta Med – volume: 275 start-page: 21960 year: 2000 end-page: 21968 article-title: Inhibition of the phosphoinositide 3‐kinase pathway induces a senescence‐like arrest mediated by p27Kip1 publication-title: J Biol Chem – volume: 53 start-page: 79 year: 2010 end-page: 88 article-title: HOMA insulin sensitivity index and the risk of all‐cause mortality and cardiovascular disease events in the general population: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) study publication-title: Diabetologia – volume: 273 start-page: 29864 year: 1998 end-page: 29872 article-title: Cyclin D expression is controlled post‐transcriptionally via a phosphatidylinositol 3‐kinase/Akt‐dependent pathway publication-title: J Biol Chem – volume: 29 start-page: 883 year: 2006 end-page: 888 article-title: Effect of sulforaphane on cell growth, G(0)/G(1) phase cell progression and apoptosis in human bladder cancer T24 cells publication-title: Int J Oncol – volume: 69 start-page: 1543 year: 2005 end-page: 1552 article-title: Role of PI3K/Akt and MEK/ERK signaling pathways in sulforaphane‐ and erucin‐induced phase II enzymes and MRP2 transcription, G2/M arrest and cell death in Caco‐2 cells publication-title: Biochem Pharmacol – volume: 10 start-page: 3 year: 1999 end-page: 10 article-title: Molecular regulation of adipocyte differentiation publication-title: Semin Cell Dev Biol – volume: 100 start-page: 44 year: 2003 end-page: 49 article-title: Mitotic clonal expansion: a synchronous process required for adipogenesis publication-title: Proc Natl Acad Sci USA – volume: 372 start-page: 108 year: 2008 end-page: 113 article-title: Vitisin A inhibits adipocyte differentiation through cell cycle arrest in 3T3‐L1 cells publication-title: Biochem Biophys Res Commun – volume: 277 start-page: 46226 year: 2002 end-page: 46232 article-title: Activation of MEK/ERK signaling promotes adipogenesis by enhancing peroxisome proliferator‐activated receptor gamma (PPARgamma) and C/EBPalpha gene expression during the differentiation of 3T3‐L1 preadipocytes publication-title: J Biol Chem – volume: 40 start-page: 229 year: 2005 end-page: 242 article-title: Adipose development: from stem cell to adipocyte publication-title: Crit Rev Biochem Mol Biol – volume: 3 start-page: 389 year: 2010 end-page: 399 article-title: Anticancer activity of a broccoli derivative, sulforaphane, in barrett adenocarcinoma: potential use in chemoprevention and as adjuvant in chemotherapy publication-title: Transl Oncol – volume: 13 start-page: 448 year: 1984 end-page: 453 article-title: Adipocyte development publication-title: Pediatr Ann – volume: 130 start-page: 3122S year: 2000 end-page: 3126S article-title: Adipocyte differentiation and gene expression publication-title: J Nutr – volume: 5 start-page: 665 year: 1989 end-page: 689 article-title: Cellular alterations in liver, skeletal muscle, and adipose tissue responsible for insulin resistance in obesity and type II diabetes publication-title: Diabetes Metab Rev – volume: 25 start-page: 83 year: 2004 end-page: 90 article-title: Sulforaphane induces caspase‐mediated apoptosis in cultured PC‐3 human prostate cancer cells and retards growth of PC‐3 xenografts in vivo publication-title: Carcinogenesis – volume: 260 start-page: 5563 year: 1985 end-page: 5567 article-title: Evidence for an increase in transcription of specific mRNAs during differentiation of 3T3‐L1 preadipocytes publication-title: J Biol Chem – volume: 22 start-page: 271 year: 2004 end-page: 275 article-title: Phase 1 study of multiple biomarkers for metabolism and oxidative stress after one‐week intake of broccoli sprouts publication-title: Biofactors – volume: 22 start-page: 7226 year: 2002 end-page: 7241 article-title: Distinct cell cycle timing requirements for extracellular signal‐regulated kinase and phosphoinositide 3‐kinase signaling pathways in somatic cell mitosis publication-title: Mol Cell Biol – volume: 396 start-page: 691 year: 2010 end-page: 695 article-title: Matrine inhibits 3T3‐L1 preadipocyte differentiation associated with suppression of ERK1/2 phosphorylation publication-title: Biochem Biophys Res Commun – volume: 271 start-page: 31372 year: 1996 end-page: 31378 article-title: Expression of a constitutively active Akt Ser/Thr kinase in 3T3‐L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation publication-title: J Biol Chem – volume: 274 start-page: 1672 year: 1996 end-page: 1677 article-title: Cancer cell cycles publication-title: Science – volume: 2 start-page: 349 year: 2001 end-page: 355 article-title: Molecular mechanisms of adipocyte differentiation publication-title: Rev Endocr Metab Disord – volume: 2 start-page: 293 year: 2003 end-page: 295 article-title: New targets for viral cyclins publication-title: Cell Cycle – start-page: 59 issue: Suppl 32–33 year: 1999 end-page: 67 article-title: Insights into the transcriptional control of adipocyte differentiation publication-title: J Cell Biochem – volume: 288 start-page: C1094 year: 2005 end-page: C1108 article-title: Antimitogenic effect of green tea (‐)‐epigallocatechin gallate on 3T3‐L1 preadipocytes depends on the ERK and Cdk2 pathways publication-title: Am J Physiol, Cell Physiol – volume: 280 start-page: C1540 year: 2001 end-page: C1554 article-title: Human intestinal epithelial cell survival: differentiation state‐specific control mechanisms publication-title: Am J Physiol, Cell Physiol – ident: e_1_2_7_15_2 doi: 10.1093/carcin/bgg178 – ident: e_1_2_7_17_2 doi: 10.4161/cc.2.4.427 – ident: e_1_2_7_36_2 doi: 10.1016/j.bbrc.2010.04.163 – ident: e_1_2_7_23_2 doi: 10.1006/scdb.1998.0276 – ident: e_1_2_7_24_2 doi: 10.1002/(SICI)1097-4644(1999)75:32 <59::AID-JCB8>3.0.CO;2-1 – ident: e_1_2_7_34_2 doi: 10.1210/en.139.4.1638 – ident: e_1_2_7_9_2 doi: 10.1023/A:1011863414321 – ident: e_1_2_7_22_2 doi: 10.1016/j.bcp.2005.03.015 – ident: e_1_2_7_5_2 doi: 10.1002/dmr.5610050804 – ident: e_1_2_7_8_2 doi: 10.1146/annurev.nu.14.070194.000531 – ident: e_1_2_7_16_2 doi: 10.1593/tlo.10235 – volume: 13 start-page: 448 year: 1984 ident: e_1_2_7_4_2 article-title: Adipocyte development publication-title: Pediatr Ann – ident: e_1_2_7_30_2 doi: 10.1055/s-0030-1270712 – ident: e_1_2_7_20_2 doi: 10.4161/cc.2.6.550 – ident: e_1_2_7_10_2 doi: 10.1152/physrev.1998.78.3.783 – ident: e_1_2_7_13_2 doi: 10.1002/biof.5520220154 – ident: e_1_2_7_32_2 doi: 10.1016/j.bbrc.2008.04.188 – ident: e_1_2_7_3_2 doi: 10.1093/eurheartj/ehp317 – ident: e_1_2_7_14_2 doi: 10.1093/jn/134.5.1134 – ident: e_1_2_7_41_2 doi: 10.1074/jbc.271.49.31372 – volume: 29 start-page: 883 year: 2006 ident: e_1_2_7_19_2 article-title: Effect of sulforaphane on cell growth, G(0)/G(1) phase cell progression and apoptosis in human bladder cancer T24 cells publication-title: Int J Oncol – ident: e_1_2_7_25_2 doi: 10.1248/bpb.33.1610 – ident: e_1_2_7_39_2 doi: 10.1074/jbc.M000759200 – ident: e_1_2_7_31_2 doi: 10.1007/s00280-005-0050-3 – ident: e_1_2_7_29_2 doi: 10.1016/j.bbrc.2008.03.129 – ident: e_1_2_7_33_2 doi: 10.1128/MCB.22.20.7226-7241.2002 – ident: e_1_2_7_28_2 doi: 10.1016/j.bbrc.2006.07.095 – ident: e_1_2_7_21_2 doi: 10.1152/ajpcell.2001.280.6.C1540 – ident: e_1_2_7_11_2 doi: 10.1167/iovs.04-1120 – ident: e_1_2_7_6_2 doi: 10.1093/jn/130.12.3122S – ident: e_1_2_7_26_2 doi: 10.1073/pnas.0137044100 – ident: e_1_2_7_27_2 doi: 10.1016/S0021-9258(18)89059-7 – ident: e_1_2_7_2_2 doi: 10.1007/s00125-009-1588-0 – ident: e_1_2_7_7_2 doi: 10.1080/10409230591008189 – ident: e_1_2_7_18_2 doi: 10.1126/science.274.5293.1672 – ident: e_1_2_7_37_2 doi: 10.1152/ajpcell.00569.2004 – ident: e_1_2_7_35_2 doi: 10.1074/jbc.M207776200 – ident: e_1_2_7_38_2 doi: 10.1074/jbc.273.45.29864 – ident: e_1_2_7_12_2 doi: 10.1016/j.phrs.2009.11.009 – ident: e_1_2_7_40_2 doi: 10.1210/endo.137.8.8754791 |
| SSID | ssj0046051 |
| Score | 2.363123 |
| Snippet | Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is... |
| SourceID | proquest pubmed crossref wiley |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 1365 |
| SubjectTerms | 3T3-L1 Cells - drug effects Adipocytes - drug effects Adipocytes - physiology Adipogenesis - drug effects Animals Anticarcinogenic Agents - pharmacology Blotting, Western Body fat Cell Cycle Checkpoints - drug effects Cell Differentiation - drug effects Cell Line Cell Proliferation - drug effects Cellular biology Humans Isothiocyanates Mice Mitosis - drug effects Obesity Phytochemicals PPAR gamma - drug effects PPAR gamma - metabolism Proliferating Cell Nuclear Antigen - drug effects Rats Thiocyanates - pharmacology Transcription Factors Up-Regulation |
| Title | Sulforaphane Inhibits Mitotic Clonal Expansion During Adipogenesis Through Cell Cycle Arrest |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1038%2Foby.2011.388 https://www.ncbi.nlm.nih.gov/pubmed/22282047 https://www.proquest.com/docview/1022150761 https://www.proquest.com/docview/1022377837 |
| Volume | 20 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVBFR databaseName: Free Medical Journals customDbUrl: eissn: 1930-739X dateEnd: 20171231 omitProxy: true ssIdentifier: ssj0046051 issn: 1930-7381 databaseCode: DIK dateStart: 19930101 isFulltext: true titleUrlDefault: http://www.freemedicaljournals.com providerName: Flying Publisher |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1tb9MwELbKkBBfEO8UBjIS8IHKXeK8OPlY2k0dowOpnTQkpChOnLVSaQptJcq_4h9yZ7tZCmUCvkSVbTWO7_H5fD7fQ8gLkTq54E7BIj8KGGg_ztJQKpbzKJAKFhhzi39wGvbP_LfnwXmj8aMWtbRaynb2fee9kv-RKpSBXPGW7D9ItvpTKIDfIF94goTh-VcyHq6mYHOm83E6wxDI8UTiMcAAJimmYe1OtZfv8BtMePSJtXrmSmInn8zLC9Rxk0VrZHl6uujD667hBa2O5uuoW62WPQCt0eEEQ6lbxh-oval5u-ZN6I5LEx6wVuXsgn2e_BLwg8qFLVYVIocmhUFvZ-OhAk00XtvW1jXhXoax7nRBGpfaZbASqtvYc5jwDGlLW9XLNMFupaO5U8OiqClcjNLbuRKYvO-lXJs0rZ4hD9xOuN3vDJMPvaPk3fHpyXatXuB5GIc6GY77av6FIVEZHuhb1pZr5DoXYYikGb3jk83ij6fMrglkMB9m71pAbw7qfdm2gn7b2mzvlLSpM7pNbtk9Cu0YwN0hDTW7S24MbBTGPfKpjju6wR21uKMGd7TCHTW4o3XcUYs7irijGnfU4O4-OTs6HHX7zLJ0sMwPA84ypISMhVvAtOdhIYtMhjKNVeDoZIBSebmIRRxEaSDzzMt5LFQWpU4huVKySL0HZG9WztQjQmFxcVUuPQfWXD9QaSyLCJqh1wu2KbFoktZm1JLMprBHJpVpokMpvCiBMU5wjBMY4yZ5WbWem9Qtf2i3vxFAYif3IkFHCO6VQrdJnlfVoHrxPA0Gt1yZNp4QkQcde2gEV70IHavc8aHmtZbklT1I3r_5yH2PP766J0_ITY7s05jW1d0ne8uvK_UUTOKlfKZB-BNm0rbb |
| linkProvider | Flying Publisher |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Sulforaphane+Inhibits+Mitotic+Clonal+Expansion+During+Adipogenesis+Through+Cell+Cycle+Arrest&rft.jtitle=Obesity+%28Silver+Spring%2C+Md.%29&rft.au=Choi%2C+Kyeong-mi&rft.au=Lee%2C+Youn-sun&rft.au=Sin%2C+Dong-mi&rft.au=Lee%2C+Seunghyun&rft.date=2012-07-01&rft.pub=Blackwell+Publishing+Ltd&rft.issn=1930-7381&rft.eissn=1930-739X&rft.volume=20&rft.issue=7&rft.spage=1365&rft_id=info:doi/10.1038%2Foby.2011.388&rft.externalDBID=HAS_PDF_LINK&rft.externalDocID=2696268401 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1930-7381&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1930-7381&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1930-7381&client=summon |