• Archives of Plastic Surgery
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• v.38 no.2
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• pp.131-134
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• 2011

Purpose: Stem cells continue to receive research attention in the clinical fields, and adipose-derived stem cells (ADSCs) have been shown to be a good source raw material. Many plastic surgeons are researching the ADSC adipogenesis with a view of conducting clinical trials, and many attempts have been made to identify the factors that promote the adipogenesis of ADSCs, but comparatively few correlation studies have been undertaken to explore the relation between reactive oxygen species (ROS) and the ADSC adipogenesis. We undertook this study is to investigate the effects of ROS on ADSC adipogenesis. Methods: ADSCs were isolated and cultured from abdominal adipose tissue, and cultured in different media; 1) DMEM(control), 2) adipogenesis induction culture medium, 3) adipogenesis induction culture medium with ROS ($20{\mu}M/50{\mu}M\;H_2O_2$), 4) adipogenesis induction culture medium containing ROS ($20{\mu}M/50{\mu}M\;H_2O_2$) and antioxidant ($10{\mu}M/20{\mu}M$ Deferoxamine). We compared adipogenesis in these different media by taking absorbance measurements after Oil-Red O staining every 5 days. Results: After culturing for 20 days, significant differences were observed between these various culture groups. Absorbance results showed significantly more adipogenesis had occurred in media containing adipogenesis induction culture medium and $H_2O_2$ (in a $H_2O_2$ dose-dependently manner) than in media containing adipogenesis induction culture medium and no $H_2O_2$ (p<0.001). Furthermore, in media containing adipogenesis induction culture medium, $H_2O_2$, and antioxidant, absorbance results were significantly lower than in adipogenesis induction culture medium and $H_2O_2$ (p<0.001). Conclusion: These findings suggest that ROS promote the adipogenesis of ADSCs. We suggests that ROS could be used in the adipose tissue engineering to improve fat cell differentiation and implantable fat tissue organization.

• Biomedical Science Letters
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• v.14 no.3
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• pp.139-146
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• 2008

The peroxisome proliferator-activated receptor ${\gamma}$ $(PPAR{\gamma})$ plays a central role in adipogenesis and lipid storage. The $(PPAR{\gamma})$ ligands, thiazolidinediones (TZDs), enhance in vitro adipogenesis in several cell types, but the role of the TZDs on in vivo adipogenesis is still poorly understood. To investigate how $PPAR{\gamma}$ ligand troglitazone regulates adipogenesis in female mice, we examined the effects of the troglitazone on adipose tissue mass, morphological changes of adipocytes, and the expression of $PPAR{\gamma}$ target and adipocyte-specific genes in low fat diet-fed female C57BL/6 mice. Administration of troglitazone for 13 weeks did not change body and total white adipose tissue weights compared with control mice. Troglitazone treatment also did not cause a significant decrease in the average size of adipocytes in parametrial adipose tissue although it is reported to increase the number of small adipocytes in male animals. Troglitazone did not affect the mRNA expression of $PPAR{\gamma}$ and its target genes as well as adipocyte-specific genes in parametrial adipose tissue. These results suggest that $PPAR{\gamma}$ does not seem to be associated with adipogenesis in females with functioning ovaries and that its inability to induce adipogenesis may be due to sex-related factors.

• BMB Reports
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• v.55 no.4
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• pp.187-191
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• 2022

Obesity is caused by an imbalance between energy intake and energy expenditure. Exercise is attracting attention as one of the ways to treat obesity. Exercise induces 'beige adipogenesis' in white adipose tissue, increasing total energy expenditure via energy dissipation in the form of heat. Also, beige adipogenesis can be induced by treatment with a beta-adrenergic receptor agonist. We developed a Cidea-dual reporter mouse (Cidea-P2A-Luc2-T2A-tdTomato, Luciferase/tdTomato) model to trace and measure beige adipogenesis in vivo. As a result, both exercise and injection of beta-adrenergic receptor agonist induced beige adipogenesis and was detected through fluorescence and luminescence. We confirmed that exercise and beta-adrenergic receptor agonist induce beige adipogenesis in Cidea-dual reporter mouse, which will be widely used for detecting beige adipogenesis in vivo.

• Biomedical Science Letters
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• v.15 no.3
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• pp.179-185
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• 2009

In our previous report, we showed that $PPAR{\gamma}$ does not influence adipogenesis in females with functioning ovaries, indicating that $PPAR{\gamma}$ activity on adipogenesis is associated with sex-related factors. Among the sex-related factors, estrogen has been recognized as a major factor in inhibiting adiposgenesis in females. Thus, we hypothensized that $17{\beta}$-estradiol (E) inhibits 3T3-L1 cell adipogenesis by preventing $PPAR{\gamma}$ activity. E decreased triglyceirde accumulation in differentiated 3T3-L1 cells compared with control group. E also decreased the expression of $PPAR{\gamma}$ mRNA as well as $PPAR{\gamma}$ dependent adipocyte-specific genes, such as adipocyte fatty acid binding protein and tumor necrosis factor $\alpha$. In addition, E not only decreased luciferase reporter activity by $PPAR{\gamma}$, but also transfection of estrogen receptor $\alpha$ ($ER{\alpha}$) or $ER{\beta}$ led to decreases in $PPAR{\gamma}$ reporter gene activation. Moreover, E-activated ERs significantly decreased the luciferase reporter gene activation induced by $PPAR{\gamma}$ transfection, suggesting that estrogen-activated ERs inhibit $PPAR{\gamma}$-dependent transactivation. Accordingly, our results demonstrate that E inhibits the action of $PPAR{\gamma}$ on adipogenesis through E activated ER, providing evidence that lack of estrogen may potentiate $PPAR{\gamma}$ action on adipogenesis.

• Journal of Microbiology and Biotechnology
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• v.26 no.11
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• pp.1836-1844
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• 2016

Adipogenesis is one of the cellular processes and a highly controlled program. Nowadays, inhibition of adipogenesis has received attention as an effective way to regulate obesity. In the current study, we investigated the inhibition effect of a chloroform extract of Pleurotus eryngii var. ferulae 'Beesan No. 2' (CEBT) on adipogenesis in 3T3-L1 murine preadipocytes. Pleurotus eryngii var. ferulae is one of many varieties of King oyster mushroom and has been reported to have various biological activities, including antitumor and anti-inflammation effects. Biological activities of 'Beesan No. 2', a new cultivar of Pleurotus eryngii var. ferulae, have not yet been reported. In this study, we found that CEBT suppressed adipogenesis in 3T3-L1 cells through inhibition of key adipogenic transcription factors, such as peroxisome proliferatoractivated receptor ${\gamma}$ and CCAAT/enhancer binding protein ${\alpha}$. Additionally, CEBT reduced the expression of the IRS/PI3K/Akt signaling pathway and its downstream factors, including mammalian target of rapamycin and p70S6 kinase, which stimulate adipogenesis. Furthermore, ${\beta}-catenin$, a suppressor of adipogenesis, was increased in CEBT-treated cells. These results indicate that Pleurotus eryngii var. ferulae 'Beesan No. 2' effectively inhibited adipogenesis, so this mushroom has potential as an anti-obesity food and drug.

• BMB Reports
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• v.54 no.2
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• pp.124-129
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• 2021

In current times, obesity is a major health problem closely associated with metabolic disease such as diabetes, dyslipidemia, and cardiovascular disease. The direct cause of obesity is known as an abnormal increase in fat cell size and the adipocyte pool. Hyperplasia, the increase in number of adipocytes, results from adipogenesis in which preadipocytes differentiate into mature adipocytes. Adipogenesis is regulated by local and systemic cues that alter transduction pathways and subsequent control of adipogenic transcription factors. Therefore, the regulation of adipogenesis is an important target for preventing obesity. Myonectin, a member of the CTRP family, is a type of myokine released by skeletal muscle cells. Although several studies have shown that myonectin is associated with lipid metabolism, the role of myonectin during adipogenesis is not known. Here, we demonstrate the role of myonectin during adipocyte differentiation of 3T3-L1 cells. We found that myonectin inhibits the adipogenesis of 3T3-L1 preadipocytes with a reduction in the expression of adipogenic transcription factors such as C/EBPα, β and PPARγ. Furthermore, we show that myonectin has an inhibitory effect on adipogenesis through the regulation of the p38 MAPK pathway and CHOP. These findings suggest that myonectin may be a novel therapeutic target for the prevention of obesity.

• Nutrition Research and Practice
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• v.15 no.3
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• pp.279-293
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• 2021

BACKGROUND/OBJECTIVES: The steamed ginger has been shown to have antioxidative effects and a protective effect against obesity. In the present study, we investigated the effects of ethanolic extract of steamed ginger (SGE) on adipogenesis in 3T3-L1 preadipocytes and diet-induced obesity (DIO) mouse model. MATERIALS/METHODS: The protective effects of SGE on adipogenesis were examined in 3T3-L1 adipocytes by measuring lipid accumulations and genes involved in adipogenesis. Male C57BL/6J mice were fed a normal diet (ND, 10% fat w/w), a high-fat diet (HFD, 60% fat w/w), and HFD supplemented with either 40 mg/kg or 80 mg/kg of SGE for 12 weeks. Serum chemistry was measured, and the expression of genes involved in lipid metabolism was determined in the adipose tissue. Histological analysis and micro-computed tomography were performed to identify lipid accumulations in epididymal fat pads. RESULTS: In 3T3-L1 cells, SGE significantly decreased lipid accumulation, with concomitant decreases in the expression of adipogenesis-related genes. SGE significantly attenuated the increase in body, liver, and epididymal adipose tissue weights by HFD. Serum total cholesterol and triglyceride levels were significantly lower in SGE fed groups compared to HFD. In adipose tissue, SGE significantly decreased adipocyte size than that of HFD and altered adipogenesis-related genes. CONCLUSIONS: In conclusion, steamed ginger exerted anti-obesity effects by regulating genes involved in adipogenesis and lipogenesis in 3T3-L1 cell and epididymal adipose tissue of DIO mice.

• International Journal of Oral Biology
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• v.43 no.1
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• pp.29-35
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• 2018

It is noted that chalcone derivatives have characteristic diverse pharmacological properties, and that precise evidence has been growing that they could regulate a tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) induced insulin resistance. The purpose of the present investigation is to elucidate the effects of the identified chalcone derivatives on adipogenesis, and to find the underlying mechanism of action in that case. Consequently, we first investigated whether the chalcone derivatives could affect the identified $PPAR{\gamma}$-induced transcriptional activity on the proliferator-activated receptor response elements (PPRE) at target promoters, and find that trans-chalcone most significantly increased the $PPAR{\gamma}$-induced transcriptional activity. Additionally, we confirmed that there were up-regulatory effects of trans-chalcone during the adipogenesis and lipid accumulation, and on the mRNA of adipogenic factors in 3T3-L1 cells. Next, we examined the effect of trans-chalcone on the inhibition induced by $TNF-{\alpha}$ on adipogenesis. To that end, we noted that the treatment with trans-chalcone attenuated the effect of $TNF-{\alpha}$ mediated secretion of various adipokines that are involved in insulin sensitivity. For this reason, we noted that this study clearly demonstrates that trans-chalcone enhanced adipogenesis, in part, by its potent effect on $PPAR{\gamma}$ activation and by its reverse effect on $TNF-{\alpha}$.

• Journal of Life Science
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• v.30 no.8
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• pp.713-721
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• 2020

Adipogenesis as a model system is needed to understand the molecular mechanisms of human adipocyte biology and the pathogenesis of obesity, diabetes, and other metabolic syndromes. Many relevant studies have been conducted with a focus on gene expression regulation and intracellular signaling relating to Peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), which are master adipogenic transcription factors. However, epigenome regulation of adipogenesis by epigenomic modifiers or histone mutations is not fully understood. Histone methylation is one of the major epigenetic modifications on gene expression in mammals, and histone H3 lysine methylation (H3Kme) in particular implicates cell differentiation during various tissue and organ development. During adipogenesis, cell type-specific enhancers are marked by histone H3K4me1 with the active enhancer mark H3K27ac. Mixed-lineage leukemia 4 (MLL4) is a major H3K4 mono-methyltransferase on the adipogenic enhancers of PPARγ and C/EBPα loci. Thus, MLL4 is an important epigenomic modifier for adipogenesis. The repressive mark H3K27me3 is mediated by the enzymatic subunit Enhancer zeste homolog 2 (EZH2) of the polycomb repressive complex 2. EZH2-mediated H3K27 tri-methylation on the Wnt gene increases adipogenesis because WNT signaling is a negative regulator of adipogenesis. This review summarizes current knowledge about the epigenomic regulation of adipogenesis by histone H3 lysine methylation which fundamentally regulates gene expression.

• Clinical and Experimental Reproductive Medicine
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• v.39 no.1
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• pp.15-21
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• 2012

Objective: Tributyltin (TBT), an endocrine disrupting chemical, has been reported to decrease ovarian function by causing apoptosis in the ovary, but the mechanism is not fully understood. Therefore, we examined whether TBT increases the expression of adipogenesis-related genes in the ovary and the increased expression of these genes is associated with apoptosis induction. Methods: Three-week-old Sprague-Dawley rats were orally administered TBT (1 or 10 mg/kg body weight) or sesame oil as a control for 7 days. The ovaries were obtained and weighed on day 8, and then they were fixed for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or frozen for RNA extraction. Using the total RNA of the ovaries, adipogenesis- and apoptosis-related genes were analyzed by real-time polymerase chain reaction (PCR). Results: The ovarian weight was significantly decreased in rats administered 10 mg/kg TBT compared to that in control rats. As determined by the TUNEL assay, the number of apoptotic follicles in ovary was significantly increased in rats administered 10 mg/kg TBT. The real-time PCR results showed that the expression of adipogenesis-related genes such as $PPAR{\gamma}$, ${\alpha}P2$, CD36, and PEPCK was increased after TBT administration. In addition, apoptosis-related genes such as $TNF{\alpha}$ and TNFR1 were expressed more in the TBT-administered rats compared with the control rats. Conclusion: The present study demonstrates that TBT induces the expression of adipogenesis- and apoptosis-related genes in the ovary leading to apoptosis in the ovarian follicles. These results suggest that the increased expression of adipogenesis-related genes in the ovary by TBT exposure might induce apoptosis resulting in a loss of ovarian function.