2012
DOI: 10.1038/oby.2011.388
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Sulforaphane Inhibits Mitotic Clonal Expansion During Adipogenesis Through Cell Cycle Arrest

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 concentra… Show more

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Cited by 86 publications
(75 citation statements)
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“…Rohitukine abrogates phosphorylation of the substrate of the AKT/mTOR pathway, 4EBP at Thr37/46, which is necessary for protein synthesis during adipogenesis. extracellular signal-regulated kinase (ERK) signaling has also been reported to be responsible for early adipogenic programming and has been the cause of inhibition of adipogenesis by C1q/ tumor necrosis factor-related protein 11 (CTRP11), suphoraphane-mediated adipogenic inhibition ( 40,41 ). In our experiments, we could not see any rohitukine-mediated alteration in this pathway.…”
Section: Discussionmentioning
confidence: 38%
“…Rohitukine abrogates phosphorylation of the substrate of the AKT/mTOR pathway, 4EBP at Thr37/46, which is necessary for protein synthesis during adipogenesis. extracellular signal-regulated kinase (ERK) signaling has also been reported to be responsible for early adipogenic programming and has been the cause of inhibition of adipogenesis by C1q/ tumor necrosis factor-related protein 11 (CTRP11), suphoraphane-mediated adipogenic inhibition ( 40,41 ). In our experiments, we could not see any rohitukine-mediated alteration in this pathway.…”
Section: Discussionmentioning
confidence: 38%
“…PPARγ up-regulation has been linked to exacerbated steatosis by the mechanism involving the activation of lipogenic genes and de novo lipogenesis and increased hepatic TG (MoranSalvador et al 2011). Recently, down-regulation of PPARγ by SF in adipocytes was confirmed by Choi et al (2012Choi et al ( , 2014. In our trial, the TG levels in blood serum were not altered, however, the TG content in the liver was decreased after the administration of both SF doses (Figure 1).…”
Section: Discussionmentioning
confidence: 53%
“…The in vivo peak concentration of 20µM SF after 50 µmol oral administration of SF (58-73 mg/kg BW) offers a clear relevance for numerous in vitro cell culture studies, where the range of 1-30µM SF was typically used (Choi et al 2012;Lee et al 2012). According to Choi et al (2012), a 6-day SF action decreased the accumulation of lipid droplets and inhibited the elevation of TG in the 3T3-L1 cells by the half-maximal inhibitory concentration 7.3µM. In our in vitro study, a short SF treatment (1.5 h) showed an inhibitory effect on basal-and insulin-stimulated lipogenesis only at the highest concentration (100µM) in isolated primary rat adipocytes (Figures 5, 6).…”
Section: Discussionmentioning
confidence: 99%
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“…This intergenerational study suggests that nutritional deprivation of pregnant women may have lasting non-genetic effects on next generation body weight. An individual epigenetic pattern is established early during gestation and is subject to transformations through environmental factors throughout life, with epigenetic mechanisms being very important in the development and transgenerational transmission of chronic non-communicable diseases (NCDs), including obesity [31,32]. Still in the maternal phase and its relation with obesity, it is the exposure in this period to several chemical products (the so-called obesogênicos), which has been associated to the increase of the BMI in the offspring, also suggesting that the obesity is being programmed prenatal or early childhood, and discontinuation of normal epigenetic regulation altering the expression of key genes is probably involved in the adipogenic pathways [33].…”
Section: Journal Of Clinical Epigenetics Issn 2472-1158mentioning
confidence: 99%