• Food Science and Biotechnology
• /
• v.17 no.2
• /
• pp.362-366
• /
• 2008

Anti-lipogenic effects of tannic acid on 3T3-L1 adipocytes as well as on rats fed high fat diet (HFD) were investigated. Tannic acid stimulated lipolysis through suppression of the leptin secretion and an increase of glycerol release in a dose dependent manner in 3T3-L1 adipocytes. For animal study, the rats were fed either HFD or HFD supplemented with 1%(w/w) tannic acid (HFDT) for 12 weeks, respectively. Body weight gain, liver weight, and visceral fat mass in rats fed HFDT were significantly decreased compared to those of rats fed HFD. The lipid profiles of HFDT group were significantly decreased compared with HFD group in the serum and liver, whereas fecal total cholesterol excretion was increased in HFDT group. These results suggest that anti-lipogenic effect of tannic acid in 3T3-L1 adipocytes and in rats fed HFD may be due to the stimulation of lipolysis and the reduction of lipid levels.

• The Journal of Internal Korean Medicine
• /
• v.37 no.3
• /
• pp.442-452
• /
• 2016

Objectives: This study was performed to investigate the anti-lipogenic effect and the mechanism of Jungmanbunso-hwan extract (JMBSH) on a cellular model of non-alcoholic fatty liver disease (NAFLD) caused by palmitate in HepG2 cells.Methods: The JMBSH was prepared, andHepG2 cells were treated with various concentrations of JMBSH in order to perform an MTT assay. The HepG2 cells were cultivated in palmitate-containing media with or without extract of JMBSH. The intracellular lipid content in the HepG2 cells was examined. The effects of JMBSH on sterol regulatory element-binding transcription factor-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and AMP-activated protein kinase (AMPK) activation in HepG2 cells were measured.Results: JMBSH did not reduce HepG2 cell viability under 1,000 μg/mL. JMBSH considerably decreased intracellular lipid accumulation caused by palmitate in HepG2 cells. JMBSH repressed expression of SREBP-1c, which mediates the induction of lipogenic genes (ACC, FAS, and SCD-1). JMBSH also activated AMPK, which plays animportant role in the regulation of hepatic lipid metabolism.Conclusions: This study suggested that JMBSH relieves hepatic steatosis by repressing SREBP-1c, which mediates the induction of lipogenic genes. The anti-lipogenic effect of JMBSH may also be related to the activation of AMPK. Therefore, JMBSH could potentially be applied to NAFLD treatment after further clinical studies.

• Proceedings of the Korean Nutrition Society Conference
• /
• 2002.11a
• /
• pp.144-144
• /
• 2002

• Journal of Nutrition and Health
• /
• v.34 no.8
• /
• pp.850-857
• /
• 2001

The study was designed to observe whether the conjugated linoleic acid supplemented to diet could reduce plasma levels of glucose and lipids which were increased in 27-weeks old Otsuka Long Evans Tokushima Fatty(OLETF) rats. Twenty male OLETF rats of 7 weeks old were fed an experimental diet containing 4.5%(w/w) total fat including 1% CLA and six of twenty rats were sacrified at 6 weeks feeding. The rest of OLETF rats was divided into 2 groups, one group was continuously fed for 14 weeks more the same experimental diet containing 1% CLA and the other group was fed control diet which eliminated CLA. CLA did not significantly reduce food intake and body weight gain in OLETF obese rats. Plasma triglyceride and total cholesterol level were significantly increased at older age of OLETF obese rats, but CLA could significantly reduce plasma cholesterol and triglyceride increased in obese rats. However, CLA was not strong enough to reduce the increased plasma glucose level and hepatic lipogenic enzyme acitivies. CLA was mostly deposited in epididymal fat pad and could be incorporated into hepatic microsomal membrane and did interfere the conversion of C18 : 0 into C18 : 1 in liver. In conclusion, CLA could have anti-atherogenic effect by reducing plasma cholesterol and triglyceride which was increased in genetically obese rats, but CLA(1%) was not good source of dietary fatty acid to reduce body fatness and plasma glucose which was increased by obese gene in older rats.

• Journal of Nutrition and Health
• /
• v.39 no.8
• /
• pp.733-741
• /
• 2006

The study was conducted to investigate the effects of dietary calcium and soy isoflavone on body fat and lipid metabolism in high fat-induced obesity. Four week old female C57/BL6J mice, known as a good model of diet-induced obesity, were fed low Ca and high fat diet for 6 weeks. After induced obesity, mice were divided into six groups according to diets varying calcium contents (0.1 or 1.5%) and genistein contents (0 or 500 or 1,000 ppm). Body weight, fat pad (perirenal fat and parameterial fat), adipocyte size, serum total lipid and total cholesterol were significantly decreased by both high Ca intake and genistein supplementation. However, the effect of genistein supplementation showed in low Ca-fed groups. Serum LDL-cholesterol and TG were significantly decreased by high Ca intake and genistein supplementation, respectively. In liver, lipogenic enzymes (fatty acid synthase and malic enzyme) activity and TG were significantly decreased by both high Ca intake and genistein supplementation. This inhibitory effect of genistein on lipogenic enzymes showed in low Ca-fed groups. But liver total cholesterol and total lipid were significantly decreased by high Ca intake and genistein supplementation, respectively. Fecal excretion of total lipid, total cholesterol and TG were significantly increased by high Ca intake, not by genistein supplementation. In conclusion, high calcium intake and genistein supplement may be beneficial for suppression of obesity through direct anti-adipogenesis by decreasing fat weight and size and indirect anti-lipo-genesis by inhibiting lipogenic enzymes activity and improving lipid profile.

• The Journal of Korean Medicine
• /
• v.41 no.4
• /
• pp.64-71
• /
• 2020

Objectives: This study was done to look into whether Nrf2 take some role in the anti-lipogenic effect of kaurenoic acid in a nonalcoholic fatty liver disease (NAFLD) cellular model. Materials and Methods: We measured the effect of kaurenoic acid on intracellular steatosis and Nrf2 activation. Next, the effect of kaurenoic acid on SREBP-1c and some lipogenic genes in palmitate treated HepG2 cells with or without Nrf2 silencing. Results: The increased SREBP-1c expression was significantly decreased by concomitant kaurenoic acid treatment in non-targeting negative control siRNA transfected HepG2 cells. However, kaurenoic acid did not significantly inhibited increased SREBP-1c level in Nrf2 specific siRNA transfected HepG2 cells Conclusions: Kaurenoic acid has a potential to activate Nrf2, which may suppress SREBP-1c mediated intracellular steatosis in HepG2 cells.

• The Journal of Internal Korean Medicine
• /
• v.35 no.2
• /
• pp.175-183
• /
• 2014

Objectives : We tried to uncover the anti-lipogenic effect and underlying mechanism of Laminaria japonica on an experimental cellular model of non-alcoholic fatty liver disease. Methods : Ethanol extract of Laminaria japonica (LJ) was prepared. Intracellular lipid content of palmitate-treated HepG2 cells was evaluated with or without LJ treatment. We measured the effects of LJ on liver X receptor ${\alpha}$ ($LXR{\alpha}$) and sterol regulatory element-binding transcription factor-1c (SREBP-1c) expression, transcription level of lipogenic genes, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and nuclear factor erythroid 2-related factor 2 (Nrf2) activation in HepG2 cells. Results : LJ markedly attenuated palmitate-induced intracellular lipid accumulation in HepG2 cells. LJ suppressed $LXR{\alpha}$-dependent SREBP-1c activation, and SREBP-1c mediated induction of ACC, FAS, and SCD-1. Furthermore, LJ activated Nrf2, which plays an important cytoprotective role in non-alcoholic fatty liver disease. Conclusions : Our study suggests that LJ has the potential to alleviate hepatic lipid accumulation, and this effect was mediated by inhibiting the $LXR{\alpha}$-SREBP-1c pathway that leads to hepatic steatosis. In addition, the anti-lipogenic potential may, at least in part, be associated with activation of Nrf2.

• Herbal Formula Science
• /
• v.24 no.2
• /
• pp.100-107
• /
• 2016

Objectives : The purpose of this study is to evaluate the anti-lipogenic effect of Sobuncheong-eum on non-alcoholic fatty liver disease in free fatty acid induced cellular model. Methods : HepG2 cells were treated with palmitate for 24h to overload intracellular triglyceride (TG) content in the presence or absence of Sobuncheong-eum extract. After palmitate treatment, Intracellular TG content was measured with TG assay kit. Several lipogenesis related markers, including AMP-activated protein kinase (AMPK), sterol regulatory element-binding transcription factor-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS), were assessed using Western-blot analyses and RT-PCR. Results : Palmitate markedly increased intracellular TG in HepG2 cells, and which were alleviated by coadministered Sobuncheong-eum extract. Sobuncheong-eum extract activated AMPK, which plays a key role in reducing hepatic lipid accumulation, and reduced lipogenic fators, SREBP-1c, ACC, and FAS. Conclusions : Taken together, it is conceivable that Sobuncheong-eum has an potential to alleviate steatosis, and which may be mediated by activating AMPK at least in part.

• Journal of Korean Medicine for Obesity Research
• /
• v.20 no.2
• /
• pp.109-121
• /
• 2020

Objectives: Tanshinone I is a bioactive constituent in Salvia miltiorrhiza. At present, the anti-obesity effect and mechanism of tanshinone I are not fully understood. Here we investigated the effect of tanshinone I on lipid accumulation in 3T3-L1 preadipocytes and zebrafish. Methods: Lipid accumulation and triglyceride (TG) content in 3T3-L1 cells were determined by Oil Red O staining and AdipoRed assay, respectively. The expression and phosphorylation levels of adipogenic/lipogenic proteins in 3T3-L1 cells were evaluated by Western blotting. The messenger RNA (mRNA) expression levels of adipogenic/lipogenic markers and leptin in 3T3-L1 cells were measured by reverse transcription polymerase chain reaction (RT-PCR). Lipid accumulation in zebrafish was assessed by LipidGreen2 staining. Results: Tanshinone I at 5 μM largely blocked lipid accumulation and reduced TG content in differentiating 3T3-L1 cells. Furthermore, tanshinone I decreased the expression of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), and perilipin A but also the phosphorylation of signal transducer and activator of transcription-3 (STAT-3) in differentiating 3T3-L1 cells. In addition, tanshinone I increased the phosphorylation of adenosine 3',5'-cyclic monophosphate (cAMP)-activated protein kinase (AMPK) while decreased the intracellular adenosine triphosphate (ATP) content with no change in the phosphorylation and expression of liver kinase-B1 in differentiating 3T3-L1 cells. Importantly, tanshinone I also reduced the extent of lipid deposit formation in developing zebrafish. Conclusions: These findings demonstrate that tanshinone I has strong anti-adipogenic effects on 3T3-L1 cells and reduces adiposity in zebrafish, and these anti-adipogenic effect in 3T3-L1 cells are mediated through control of C/EBP-α, PPAR-γ, STAT-3, FAS, ACC, perilipin A, and AMPK.

• YAKHAK HOEJI
• /
• v.56 no.1
• /
• pp.1-8
• /
• 2012

In this study, we investigated the anti-obese activity of sevennight extract in high fat diet-ob/ob C57BL/6J mice by oral administered for 1 weeks. Mate water extract (MATEWi) was found to lower whole body and epididymal adipose tissue weights and lowered plasma levels of triglyceride (TG) and total cholesterol (TC), HDL and LDL, compared to those in high fat fed ob/ob group. These results suggest that Mate extract ameliorates obesity through activation of lipogenic enzymes and FA oxidation resulting from phosphorylation of AKT and GSK-$3{\beta}$, and could be developed as a potential therapeutic agent for obese mices.