• Title/Summary/Keyword: Decrease of Lipid Accumulation

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TR4 Inhibits LXR-mediated Decrease of Lipid Accumulation in 3T3-L1 Adipocytes

  • Choi, Ho-Jung;Kim, Eung-Seok
    • Food Science of Animal Resources
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    • v.31 no.3
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    • pp.398-404
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    • 2011
  • TR4 has been suggested to play an important role in lipid metabolism in adipocytes. Although TR4 facilitates lipid accumulation during adipogenesis, the regulatory effect of TR4 on lipid storage in mature adipocytes remains unclear. We showed that TR4 inhibited the LXR agonist GW3965-mediated decrease of lipid accumulation in 3T3-L1 adipocytes. A reporter gene analysis revealed that TR4 suppressed LXR${\alpha}$ transcriptional activity, although LXR${\alpha}$ was unable to affect TR4 transcriptional activity. Moreover, adding TR4 resulted in reduced LXR${\alpha}$ binding to the LXR responsive element in a gel shift assay. Additionally, the suppressive effect of GW3965 on perilipin expression and lipid accumulation in 3T3-L1 adipocytes was abolished by TR4 overexpression. Taken together, our data demonstrate that TR4 plays an inhibitory role in LXR${\alpha}$-mediated suppression of lipid accumulation in 3T3-L1 adipocytes. This TR4 protective effect is mediated, in part, y blocking the suppressive effect of GW3965 on perilipin gene expression.

Dietary Niacin Supplementation Suppressed Hepatic Lipid Accumulation in Rabbits

  • Liu, Lei;Li, Chunyan;Fu, Chunyan;Li, Fuchang
    • Asian-Australasian Journal of Animal Sciences
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    • v.29 no.12
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    • pp.1748-1755
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    • 2016
  • An experiment was conducted to investigate the effect of niacin supplementation on hepatic lipid metabolism in rabbits. Rex Rabbits (90 d, n = 32) were allocated to two equal treatment groups: Fed basal diet (control) or fed basal diet with additional 200 mg/kg niacin supplementation (niacin). The results show that niacin significantly increased the levels of plasma adiponectin, hepatic apoprotein B and hepatic leptin receptors mRNA (p<0.05), but significantly decreased the hepatic fatty acid synthase activity and adiponectin receptor 2, insulin receptor and acetyl-CoA carboxylase mRNA levels (p<0.05). Plasma insulin had a decreasing tendency in the niacin treatment group compared with control (p = 0.067). Plasma very low density lipoproteins, leptin levels and the hepatic adiponectin receptor 1 and carnitine palmitoyl transferase 1 genes expression were not significantly altered with niacin addition to the diet (p>0.05). However, niacin treatment significantly inhibited the hepatocytes lipid accumulation compared with the control group (p<0.05). In conclusion, niacin treatment can decrease hepatic fatty acids synthesis, but does not alter fatty acids oxidation and triacylglycerol export. And this whole process attenuates lipid accumulation in liver. Besides, the hormones of insulin, leptin and adiponectin are associated with the regulation of niacin in hepatic lipid metabolism in rabbits.

Glucosamine increases macrophage lipid accumulation by regulating the mammalian target of rapamycin signaling pathway

  • Sang-Min Kim;Dong Yeol Kim;Jiwon Park;Young-Ah Moon;Inn-Oc Han
    • BMB Reports
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    • v.57 no.2
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    • pp.92-97
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    • 2024
  • Elevated blood glucose is associated with an increased risk of atherosclerosis. Data from the current study showed that glucosamine (GlcN), a normal glucose metabolite of the hexosamine biosynthetic pathway (HBP), promoted lipid accumulation in RAW264.7 macrophage cells. Oleic acid- and lipopolysaccharide (LPS)-induced lipid accumulation was further enhanced by GlcN in RAW264.7 cells, although there was no a significant change in the rate of fatty acid uptake. GlcN increased acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), scavenger receptor class A, liver X receptor, and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression, and; conversely, suppressed ATP-binding cassette transporter A1 (ABCA-1) and ABCG-1 expression. Additionally, GlcN promoted O-GlcNAcylation of nuclear SREBP-1 but did not affect its DNA binding activity. GlcN stimulated phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-specific inhibitor, suppressed GlcN-induced lipid accumulation in RAW264.7 cells. The GlcN-mediated increase in ACC and FAS mRNA was suppressed, while the decrease in ABCA-1 and ABCG-1 by GlcN was not significantly altered by rapamycin. Together, our results highlight the importance of the mTOR signaling pathway in GlcN-induced macrophage lipid accumulation and further support a potential link between mTOR and HBP signaling in lipogenesis.

The Degree of Lipid Oxidation of Rat Liver Fed Peroxidized Lipid and Its Effects on Anti-Oxidative System (과산화지질의 투여가 흰쥐 간의 산화와 항산화계에 미치는 영향)

  • 권명자;전영수;송영옥
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.23 no.6
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    • pp.899-907
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    • 1994
  • Accumulation of peroxidized lipid, fed or injected in the body of rats was investigated and the effect of peroxidized lipid on the antioxidative system was studied also. Three groups each having six of Sprague-dawley rats were raised for 8 weeks. the peroxide value(POV) of diet fed to the control and the peroxidized group was 5.47 and 22.14meq/kg , respectively. Injected group was given the control diet and peroxidized linoleic acid(POV 31.81meq/kg) was injected into the peritoneal area three times a week. The POV, MDA, and protein carbonyl values of the peroxidized and the injected group (experimental groups) were significantly higher (p<0.05) than those of the control group. Cu, Zn-SOD and M-SOD activity of the experimentla groups increased 1.6 times that of control group at 4 th week. and decreased by 60% of their activityafter 8 weeks of feeding (p<0.05) . Catalase activity, glutathione and Vt, E contents of the experimental groups were significantly lower (p<0.05) than those of the control group during 8 weeks. The accumulation of peroxidcized lipid in liver were ovserved both in the fed or the injected group. The increased of enzyme activity of the experimental group during 4 weeks suggests ianadaptation of antioxidative system to get rid of the peroxidized lipid. Decrease of enzyme activity and glutathione observed as the peroxidized lipid lipid accumulation proceeded further, however, seems to indicate the oxdiative damage of enzyme and protein . Determination of the protein carbonyl content may be used as a method for measuring the oxidative damaging effect of peroxidized lipid.

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UV-induced Mutagenesis of Nannochloropsis oculata for the Increase of Lipid Accumulation and its Characterization (자외선 조사에 의한 Nannochloropsis oculata의 지질 축적량 향상 변이주 생성 및 특성 분석)

  • Kim, Jong-Hun;Park, Hyun-Jin;Kim, Young-Hwa;Joo, Hyun;Lee, Sang-Hoon;Lee, Jae-Hwa
    • Applied Chemistry for Engineering
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    • v.24 no.2
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    • pp.155-160
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    • 2013
  • Research on mutant generation and isolation for microalgae yielding enhanced lipid accumulation is an important issue for the production of economic biodiesel. In the present study, ultraviolet (UV-B type) ray induced mutant generation was tried using a photosynthetic microalgae, Nannochloropsis oculata (N. oculata), for the production of biodiesel. The resulting colonies were isolated and further cultured with both liquid and solid state f/2 media. After a few week cultivation, changes of cell growth rate, dry cell weight, and several important intracellular components (chlorophyll, carotenoid, and lipid) were investigated. Two mutants among thousands colonies showed an increased cell growth and high lipid accumulation as compared to those of wild type. It was also observed that the increased cell growth rate is associated with the overexpressed intracellular proteins. However, the mutants showed a decrease in the chlorophyll biosynthesis.

Inhibitory Effect of Heartwood of Rhus verniciflua Stokes on Lipid Accumulation in 3T3-L1 Cells (3T3-L1 세포에 대한 옻나무 추출물의 지방축적 억제효과)

  • Kim, Se-Gun;Rhyu, Dong-Young;Kim, Do-Kuk;Ko, Da-Hyung;Kim, Yun-Kyung;Lee, Young-Mi;Jung, Hyun-Ju
    • Korean Journal of Pharmacognosy
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    • v.41 no.1
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    • pp.21-25
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    • 2010
  • The MeOH extract of Rhus verniciflua heartwood inhibited lipid accumulation in 3T3-L1 adipocytes. Chromatographic methods including of silica gel, RP-18 and high-pressure liquid chromatography isolated sulfuretin and fisetin from the extract as active constituents. The isolated compounds, especially sulfuretin, strongly inhibited lipid accumulation in adipocytes. The treatment of sulfuretin and fisetin led to decreased expression of peroxisome proliferator-activated receptor-gamma ($PPAR{\gamma}$), as an important transcription factor in fat cell differentiation, which was equal to the decrease in the quercetin positive control. The presence of a hydroxyl group (C-5) in quercetin compared to fisetin, and the presence of C-2 double bonds in fisetin compared with fustin increased the inhibitory effect of lipid accumulation.

Protective Effect of Isoliquiritigenin against Ethanol-Induced Hepatic Steatosis by Regulating the SIRT1-AMPK Pathway

  • Na, Ann-Yae;Yang, Eun-Ju;Jeon, Ju Mi;Ki, Sung Hwan;Song, Kyung-Sik;Lee, Sangkyu
    • Toxicological Research
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    • v.34 no.1
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    • pp.23-29
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    • 2018
  • Ethanol-induced fat accumulation, the earliest and most common response of the liver to ethanol exposure, may be involved in the pathogenesis of liver diseases. Isoliquiritigenin (ISL), an important constituent of Glycyrrhizae Radix, is a chalcone derivative that exhibits antioxidant, anti-inflammatory, and phytoestrogenic activities. However, the effect of ISL treatment on lipid accumulation in hepatocytes and alcoholic hepatitis remains unclear. Therefore, we evaluated the effect and underlying mechanism of ISL on ethanol-induced hepatic steatosis by treating AML-12 cells with 200 mM ethanol and/or ISL ($0{\sim}50{\mu}M$) for 72 hr. Lipid accumulation was assayed by oil red O staining, and the expression of sirtuin1 (SIRT1), sterol regulatory element-binding protein-1c (SREBP-1c), AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor alpha ($PPAR{\alpha}$) was studied by western blotting. Our results indicated that ISL treatment upregulated SIRT1 expression and downregulated SREBP-1c expression in ethanol-treated cells. Similarly, oil red O staining revealed a decrease in ethanol-induced fat accumulation upon co-treatment of ethanol-treated cells with 10, 20, and $50{\mu}M$ of ISL. These findings suggest that ISL can reduce ethanol induced-hepatic lipogenesis by activating the SIRT1-AMPK pathway and thus improve lipid metabolism in alcoholic fatty livers.

Effects of Chestnut Inner Shell Extract on 3T3-L1 Preadipocyte Differentiation (율피 추출물이 3T3-L1 지방전구세포 분화에 미치는 영향)

  • Lee, Seon-Goo
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.24 no.2
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    • pp.266-271
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    • 2010
  • Obesity occurred by energy imbalance, is increasing regardless of race, sex, age, and related to the metabolic syndrome, diabetes and cardiovascular disease. Since adipose tissue plays a critical role in regulating energy homeostasis, understanding of adipogenesis pathway and finding of regulatory mechanism for adipogenesis can be helpful to manage obesity as well as obesity-related diseases. In this study, to investigate the effects of Chestnut Inner Shell(CIS) extract on the adipogenesis in 3T3-L1 preadipocytes, 3T3-L1 preadipocytes were differentiated with adipogenic reagents for 9 days in the absence or presence of CIS extract ranging from 10 - 100 ${\mu}g/m{\ell}$. The effect of CIS extract on 3T3-L1 differentiation was examined by measuring intracelluar lipid droplet and triglyceride contents. CIS extract remarkably inhibited lipid accumulation(about 45% inhibition at 100 ${\mu}g/m{\ell}$ of CIS extract) and slightly decreased triglyceride contents(about 15% decrease at 100 ${\mu}g/m{\ell}$ of CIS extract) in 3T3-L1 preadipocytes at the concentration showing no cytotoxicity. These results demonstrated that CIS extract significantly inhibit adipogenesis and can be used for the regulation of obesity.

The Antihyperlipidemic Effect of Colpomenia bullosa Extract -Based on the Decreasing Effect of Lipid Accumulation in Hepatocyte of Murine with Hyperlipidemia induced by Triton WR-1339 (긴볼레기말의 항고지혈증 효과에 관한 연구 - Triton WR-1339 주사에 의한 고지혈증 유발 생쥐의 간세포내 지방 축적 감소를 중심으로)

  • Park, In-Sick;Ahn, Sang-Hyun;Chung, Jae-Man;Kang, Yun-Ho;Lee, Hai-Poong;Seo, Gwi-Moon;Hong, Young-Ki;Kim, Ho-Hyun;Kim, Jin-Tack
    • The Journal of Dong Guk Oriental Medicine
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    • v.7 no.2
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    • pp.97-105
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    • 1999
  • Hepatic tissues of ICR mouse were intraperitoneally injeced with Colpomenia bullosa(CB) Extract after Triton WR-1339(TX) injection were observed to investigate the antihyperlipermic effect of CB extract for hyperlipidemic hepatic tissue caused by destruction of lipid metabolism. The hepatic tissues were obtained at hour-24, 48, and 72 after TX injection with CB extract treatment. And then these specimen were fixed in 10% neutral buffer solution and were cryocut. The tissue stained by H&E for general morphology and sudan black B for lipid distribution. The increase of hepatocyte havinig meshlike cytoplasm were shown in all hepatic lobules after TX injection and the hepatic plates were disappeared in the region of meshlike hepatocyte aggregation. But the hepatocyte having meshlike cytoplasm were disappeared and hapatic plate were rearranged in CB extract injected mouse. The number of blue black colored lipid drop in hepatic cytoplasm of mouse injected with TX were increased and the size of lipid drop were enlarged. But the number of lipid drop in hepatic cytoplasm of mouse treated CB extract were decreased and the size of lipid drop were diminished. As results indicated that the accumulation of lipid drop caused by TX injection were mitigated by the antihyperlipidermic effect of CB extract.

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The micosporine-like amino acids-rich aqueous methanol extract of laver (Porphyra yezoensis) inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes

  • Kim, Hyunhee;Lee, Yunjung;Han, Taejun;Choi, Eun-Mi
    • Nutrition Research and Practice
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    • v.9 no.6
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    • pp.592-598
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    • 2015
  • BACKGROUND/OBJECTIVES: Increased mass of adipose tissue in obese persons is caused by excessive adipogenesis, which is elaborately controlled by an array of transcription factors. Inhibition of adipogenesis by diverse plant-derived substances has been explored. The aim of the current study was to examine the effects of the aqueous methanol extract of laver (Porphyra yezoensis) on adipogenesis and apoptosis in 3T3-L1 adipocytes and to investigate the mechanism underlying the effect of the laver extract. MATERIALS/METHODS: 3T3-L1 cells were treated with various concentrations of laver extract in differentiation medium. Lipid accumulation, expression of adipogenic proteins, including CCAAT enhancer-binding protein ${\alpha}$, peroxisome proliferator-activated receptor ${\gamma}$, fatty acid binding protein 4, and fatty acid synthase, cell viability, apoptosis, and the total content and the ratio of reduced to oxidized forms of glutathione (GSH/GSSG) were analyzed. RESULTS: Treatment with laver extract resulted in a significant decrease in lipid accumulation in 3T3-L1 adipocytes, which showed correlation with a reduction in expression of adipogenic proteins. Treatment with laver extract also resulted in a decrease in the viability of preadipocytes and an increase in the apoptosis of mature adipocytes. Treatment with laver extract led to exacerbated depletion of cellular glutathione and abolished the transient increase in GSH/GSSG ratio during adipogenesis in 3T3-L1 adipocytes. CONCLUSION: Results of our study demonstrated that treatment with the laver extract caused inhibition of adipogenesis, a decrease in proliferation of preadipocytes, and an increase in the apoptosis of mature adipocytes. It appears that these effects were caused by increasing oxidative stress, as demonstrated by the depletion and oxidation of the cellular glutathione pool in the extract-treated adipocytes. Our results suggest that a prooxidant role of laver extract is associated with its antiadipogenic and proapoptotic effects.