Jo, Hyun Kyun;Han, Min Ho;Hong, Su Hyun;Choi, Yung Hyun;Park, Cheol
Journal of Life Science
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v.25
no.3
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pp.285-292
/
2015
Citrus peel (CP) is used as a traditional herb with diverse beneficial pharmacological activities, such as anti-inflammatory, anti-oxidant, and anti-allergic effects. However, the anti-obesity effects of citrus peel are poorly defined. The aim of this study was to evaluate ethanol extracts of citrus peel (EECP) for its adipocyte differentiation and adipogenesis in 3T3-L1 preadipocytes. The aim of this study was to evaluate an EECP for its adipocyte differentiation and adipogenesis in 3T3-L1 preadipocytes. Treatment with EECP significantly suppressed the terminal differentiation of 3T3-L1 preadipocytes in a dose-dependent manner, as confirmed by a decrease in lipid droplet number and lipid content and an accumulation of cellular triglyceride. EECP exhibited potential adipogenesis inhibition and downregulated the expression of pro-adipogenic transcription factors, such as sterol regulatory elementbinding protein-1c (SREBP-1c), peroxisome proliferator-activated receptor-γ (PPARγ), CCAAT/enhancerbinding proteins α (C/EBPα) and C/EBPβ, and adipocyte expressed genes, such as adipocyte fatty acid binding protein (aP2) and Leptin. In addition, EECP treatment effectively activated the AMP-activated protein kinase (AMPK) signaling pathway; however, compound C, a specific inhibitor of AMPK, significantly reduced the EECP-induced inhibition of adipogenesis. Taken together, these results indicate EECP showed strong anti-obesity effects through the AMPK signaling pathway, and further studies will be needed to identify the active compounds that confer the anti-obesity activity of EECP.
BACKGROUND/OBJECTIVES: Psidium guajava L. (guava) leaves have been shown to exhibit hypoglycemic and antidiabetic effects in rodents. This study investigated the effects of guava leaf extract on adipogenesis, glucose uptake, and lipolysis of adipocytes to examine whether the antidiabetic properties are mediated through direct effects on adipocytes. MATERIALS/METHODS: 3T3-L1 cells were treated with 25, 50, 100 ㎍/mL of methanol extract from guava leaf extract (GLE) or 0.1% dimethyl sulfoxide as a control. Lipid accumulation was evaluated with Oil Red O Staining and AdipoRed assay. Immunoblotting was performed to measure the expression of adipogenic transcription factors, fatty acid synthase (FAS), and AMP-activated protein kinase (AMPK). Glucose uptake under basal or insulin-stimulated condition was measured using a glucose analog 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose. Lipolysis from fully differentiated adipocytes was measured by free fatty acids release into the culture medium in the presence or absence of epinephrine. RESULTS: Oil Red O staining and AdipoRed assay have shown that GLE treatment reduced lipid accumulation during adipocyte differentiation. Mitotic clonal expansion, an early essential event for adipocyte differentiation, was inhibited by GLE treatment. GLE inhibited the expression of transcription factors involved in adipocyte differentiation, such as peroxisome proliferator-activated receptor 𝛄 (PPAR𝛄), CCAAT/enhancer-binding protein α (C/EBPα), and sterol regulatory element-binding protein-1c (SREBP-1c). FAS expression was also decreased while the phosphorylation of AMPK was increased by GLE treatment. In addition, GLE increased insulin-induced glucose uptake into adipocytes. In lipid-filled mature adipocytes, GLE enhanced epinephrine-induced lipolysis but reduced basal lipolysis dose-dependently. CONCLUSIONS: The results show that GLE inhibits adipogenesis and improves adipocyte function by reducing basal lipolysis and increasing insulin-stimulated glucose uptake in adipocytes, which can be partly associated with antidiabetic effects of guava leaves.
Na Gyeong Geum;Jeong Won Choi;Hyeok Jin Choi;Gwang Hyeon Ryu;Jin Boo Jeong
Korean Journal of Plant Resources
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v.36
no.6
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pp.541-548
/
2023
In the present study, the effects of HML on lipolysis, adipocyte browning, autophagy, and proliferation were investigated. HML affected lipolysis by increasing the protein levels of ATGL and HSL, and phosphorylation levels of HSL and AMPK. Furthermore, HSL decreased the perilipin-1 levels. In addition, free glycerol content was increased by HML treatment. HML affected adipocyte browning by increasing the protein levels of UCP-1, PGC-1α, and PRDM16. In addition, HML affected autophagy by increasing the levels of LC3-I and LC3-II, and decreasing those of SQSTM1/p62. Moreover, HML affected adipocyte proliferation by suppressing the proliferation of 3T3-L1 cells due to arrest of the cell cycle via blocking the expression of β-catenin and cyclin D1. These results suggest that HML induces lipolysis, adipocyte browning, autophagy, and inhibits excessive proliferation of adipocytes.
Objectives : Daesiho-tang (DSHT) has been widely used in the treatment of cerebral infarct in traditional medicine. However, there was not report on the anti-obesity-related diseases efficacy of DSHT. In this study, we investigated the effects for the new formulation of DSHT, on the adipocyte differentiation cycle in 3T3-L1 cells. Methods : 3T3-L1 cells were treated with DSHT (50, 100, $200{\mu}g/m{\ell}$) during differentiation for 6 days. Also, the inhibitory effect of DSHT against 3T3-L1 adipogenesis was evaluated in various stage of adipogenesis such as early (0-2day), intermediate (2-4day), and terminal stage (4-6day). The accumulation of lipid droplets was determined by Oil Red O staining. and, the expressions of genes related to adipogenesis were measured by RT-PCR and Western blot analyses. Results : DSHT showed inhibitory activity on adipocyte differentiation at 3T3-L1 preadipocytes without affect cell toxicity as assessed by measuring fat accumulation and adipogenesis. In addition, DSHT significantly reduced the expression levels of several adipocyte marker genes including proliferator activated $receptor-{\gamma}$ ($PPAR-{\gamma}$) and CCAAT/ enhancer-binding $protein-{\alpha}$ ($C/EBP-{\alpha}$). Also, the anti-adipogenic effect of DSHT was strongly limited in the intermediate (2-4 day), terminal stage (4-6 day) of 3T3-L1 adipogenesis. In addition, the DSHT treatment down- regulated mRNA expression levels of $PPAR-{\gamma}$,, $C/EBP-{\alpha}$ in mature 3T3-L1 adipocytes. Conclusions : These results suggest that, the ability of DSHT has inhibited overall adipogenesis and lipid accumulation in the 3T3-L1 cells. The new formulation of DSHT may be a promising medicine for the treatment of obesity and related metabolic disorders.
The purpose of this study was to find out effects of treatment of ginsenoside Re, Rc and EGCG on mRNA expressions of leptin, hormone sensitive lipase (HSL) and resistin in 3T3-L1 adipocytes. The concentrations of EGCG were treated with $0.01{\times}10^{-7},\;0.1{\times}10^{-7},\;1{\times}10^{-7}\;and\;1{\times}10^{-6}\;or\;100{\mu}g/ml$ ginsenoside Re, Rc in culture cell for 13 days. mRNA expression of leptin wasn't expressed in preadipocyte but according to differentiation of adipocyte, the that of mRNA expression was decreased at gensenosids or EGCG treated cells compared with non treated adipocyte. Expression of HSL mRNA was increased in G-Re, G-Rc and EGCG treated cells compared with non treated cells. The resistin level was significantly decreased in adipocytes treated with G-Re, G-Rc and EGCG. These pattern was similar to leptin expression. These results support that treatment of gensenosides or EGCG in 3T3-L1 adipocyte resulted to affect of leptin and resistin as well as HSL mRNA levels, accordingly, levels of leptin and HSL will be acted by signalling body fat stores to the hypothalamus which in turn regulates food intake andenergy expenditure to maintain body weight homeostasis. And also regulation of resistin mRNA will prevent to diabetics attacked with obesity. In conclusion, we suggest that consumption of ginseng saponine or EGCG might prevent human diabetics or/and obesity.
Choi, Jae Young;Lim, Jong Seok;Sim, Bo Ram;Yang, Yung Hun
Journal of Life Science
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v.30
no.6
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pp.532-541
/
2020
In this study, we describe the inhibition of adipocyte differentiation by the lactic acid bacteria (LAB) fermentation product of Chrysanthemum indicum L. (CI) extract to control obesity. Preparation of LAB-fermented products was performed to overcome the cytotoxicity of CI extract. During fermentation and 3T3-L1 cell line experiment, cytotoxicity was not induced in the CI fermentation products over 1 day in culture. Fermented materials from highly proliferative cultures were selected for treatment of 3T3-L1 cells and for comparison with unfermented control groups. Cell survival and undifferentiated cell populations were decreased differentiation population in all experimental groups compared with controls, as measured using fluorescence-activated cell sorting analysis. Akt pathway activity increased upon treatment with these fermented extracts in 3T3-L1 cells. Gli2 depleted at the protein level in association with adipocyte differentiation. LAB KCTC 3115- and 3109-fermented extract treatment caused controlled Gli2 protein accumulation. Moreover, KCTC 3115 and 3109 were found to reduce C/EBPα and FAS was depleted, whereas pACC was increased at the protein level upon treatment with the fermentation products of each of the four LAB used in this study. With Lactococcus lactis subsp. lactis KCTC 3115 fermentation, the regulation of adipose differentiation and hedgehog signaling were also suppressed, thereby inhibiting the differentiation of progenitor cells. The basis for the activation of hedgehog signaling may provide insights into the treatment of obesity and the inhibition of adipocyte differentiation.
Effects of perilla leaf extracts (PLE) on adipocytes differentiation of 3T3-L1 cells were examined. Ethanol extract of PLE treatment significantly decreased lipid accumulation, a marker of adipogenesis, in a dose-dependent manner. Moreover, gene expression levels of peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$), the key adipogenic transcription factor, were markedly decreased by PLE. PLE also suppressed adipocyte fatty acid binding protein (aP2) and glycerol-3-phosphate dehydrogenase (GPDH), which are adipogenic marker proteins. These results suggest that PLE treatment suppressed differentiation of 3T3-L1 adipocytes, in part by down-regulating expression of adipogenic transcription factor and other specific target genes.
Objective This study was designed to investigate the effects of Gamiygin-tang (GY) extract (GYE) and fermented solution (GYF) on body weight, serum lipid level and adipocyte differentiation in high fat diet-fed obese mice. Materials and Methods High fat diet-fed obese mice and 3T3-L1 adipocytes mice were treated with GYE and GYF and obesity related markers were assessed. A cytotoxicity assay was carried out by MTS assay. Inhibitory effects of GYE and GYF on adipocyte differentiation were carried out by Oil Red O staining. The effects of GYE and GYF on the expression of adipocyte differentiation regulatory factors, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and CCAAT/enhancer binding protein alpha (CEBP-${\alpha}$) were measured by real-time reverse transcriptase-polymerase chain reaction. The effects of GYE and GYF on the expression of adipocyte differentiation regulatory factors were also determined in relation to protein production/protein levels by western blotting. The anti obesity effects of GYE and GYF were measured in high fat-diet induced obese mice. Various factors were measured from the serum of the high fat-diet mice. Results Though GYE did not show toxicity at the concentration of 1mg/ml, GYF showed toxicity at the concentration of 1mg/ml. The GYE at 0.1 and 1mg/ml inhibited the differentiation of 3T3-L1 cells, and the GYF also inhibited the differentiation of 3T3-L1 cells. The effect of GYE on adipocyte differentiation factors including PPAR-${\gamma}$ and CEBP-${\alpha}$ was investigated and compared to the corresponding concentration levels of GYF. GYE and GYF both suppressed the RNA and protein levels of adipocyte differentiation factors. In the animal test both GYE and GYF reduced weight gain. GYE and GYF reduced blood cholesterol, TG and LDL levels. GYF better reduced blood cholesterol levels. Conclusions These results demonstrate that GYE and GYF exerts anti-obesity effect in 3T3-L1 cells and obese mice induced by high-fat diet.
Up until today, the key to contouring has been resumed in these two alternatives, either limiting the adipocyte storing capacity by modulating lipogenesis, or by stimulating lipolysis to eliminate adipocyte lipid content. Another interesting way could be the regulation of adipocyte differentiation. In this work, we have evaluated the effect of a brown algal extract of Sphacelaria scoparia (SSE) on the differentiation of pre-adipocytes into adipocytes. A pre-adipocyte line (3T3-L 1) was used. The differentiation was evaluated by the measure of produced lipids thanks to red oil coloration and spectrophotometry, and also by the expression of adipocyte differentiation markers: enzymes such as fatty acid synthase (FAS) and stearoyl CoA desaturase (SCD), or membrane proteins such as glucose transporters (GLUT -4) and fatty acid transporters (FAT) expressed on the surface of human adipocytes. These genes are under control of two transcription factors: CAAT-enhancer binding protein (c/EBP alpha) and sterol response element binding protein (SREBP1). All these markers were analysed at different stages of differentiation by RT -PCR. Sphacelaria extract (SSE) inhibits pre-adipocytes differentiating into adipocytes following a dose-dependant relation, using a kinetics similar to retinoic acid. It decreases the expression of mRNA specific to FAS, FAT, GLUT -4, SCD1, c/EBP alpha and SREBP1. Moreover, SSE regulated on collagen 1 and collagen 4 expression. A stimulation of collagen 1 was also measured in human skin fibroblasts. Thus, SSE performs as a genuine differentiation inhibitor and not only as a lipogenesis inhibitor, and could be used in slimming products.
Undaria pinnatifada has been used as a natural diet food with few calories and as a source of iodine. Even though U. pinnatifida has been regarded as a diet food, the mechanisms of its inhibitory effects on adipocyte differentiation and the accumulation of fat in adipocytes are poorly understood. In this study, the effect and mechanism of U. pinnatifida ethanol extract on 3T3-L1 differentiation into adipocytes were investigated. The effects of U. pinnatifida ethanol extract on cell viability and the anti-adipogenic effect were investigated via MTT assay, Oil red O staining, RT-PCR, and western blot. The U. pinnatifida ethanol extract did not show toxicity up to a concentration of 50 ${\mu}g/ml$. The addition of U. pinnatifida ethanol extract decreased triglyceride contents by 40% when 50 ${\mu}g/ml$ of U. pinnatifida ethanol extract was added during 3T3-L1 differentiation and adipocyte triglyceride formation. The transcription and expression of peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$), leptin, and hormone-sensitive lipase (HSL) as adipocyte-specific proteins were determined by RT-PCR and western blot. The overexpression of $PPAR{\gamma}$ could accelerate adipocyte differentiation. Also, leptin was secreted for triglyceride accumulation in the adipocytes and the increase of adipocyte cell size. Thus, $PPAR{\gamma}$ and leptin were used as indicators of obesity. $PPAR{\gamma}$ and leptin were repressed by the increased addition of U. pinnatifida ethanol extract. This indicates that U. pinnatifida was effective as an anti-obesity agent by repressing the differentiation of 3T3-L1 into adipocytes and inhibiting triglyceride formation in adipocytes.
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