• Proceedings of the SCSK Conference
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• 2003.09a
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• pp.440-447
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• 2003

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.

• Journal of Plant Biotechnology
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• v.1 no.1
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• pp.20-30
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• 1999

In order to modify lipid production of Perilla qualitatively as well as quantitatively by genetic engineering, genes involved in carbon metabolism were isolated and characterized. These include acyl-ACP thioesterases from Perilla frutescens and Iris sp., four different $\beta$-ketoacyl- ACP synthases from Perilla frutescens, and two $\Delta$15 a-cyl-ACP desaturases(Pffad7, pffad3). Δ15 acyl-ACP desa turase (Δ15-DES) is responsible for the conversion of linoleic acid (18:2) to $\alpha$-linolenic acid (ALA, 18:3). pffad 3 encodes Δ15 acyl-desaturase which is localized in ER membrane. On the other hand, Pffad7 encodes a 50 kD plastid protein (438 residues), which showed highest sequence similarity to Sesamum indicum fad7 protein. Northern blot analysis revealed that the Pffad7 is highly expressed in leaves but not in roots and seeds. And Pffad3 is expressed throughout the seed developmental stage except very early and fully mature stage. We constructed Pffad7 gene under 355 promoter and Pffad3 gene under seed specific vicillin promoter. Using Pffad7 construct, Perilla, an oil seed crop in Korea, was transformed by Agrobacterium leaf disc method. $\alpha$-linolenic acid contents increased in leaves but decreased in seeds of transgenic Perilla. Currently, we are transforming Perilla with Pffad3 construct to change Perilla seed oil composition. We isolated three ADP-glucose pyrophosphorylase (AGP) genes from Perilla immature seed specific cDNA library. Nucleotide sequence analysis showed that two of three AGP (Psagpl, Psagp2) genes encode AGP small subunit polypeptides and the remaining (Plagp) encodes an AGP large subunit. PSAGPs, AGP small subunit peptide, form active heterotetramers with potato AGP large subunit in E. coli expressing plant AGP genes.

• The Journal of Korean Medicine
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• v.36 no.4
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• pp.74-79
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• 2015

Objectives: Here we investigated the anti-lipogenic potential of kaurenoic acid (KA), a diterpene derived from Aralia continentalis, in a cellular model of non-alcoholic fatty liver disease. Methods: HepG2 cells were treated with palmitate for 24h to induce intracellular lipid accumulation. To assess the influence of KA on steatotic HepG2 cells, various concentration of KA was co-administered. After palmitate treatment, Intracellular triglyceride content was measured. Expression level of several lipogenic genes, sterol regulatory element-binding transcription factor-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD-1) were measured using Western-blot analyses or RT-PCR. Results: Palmitate markedly increased intracellular triglyceride level and expression of related lipogenic genes in HepG2 cells, and which was relieved by co-administered KA. Conclusions: It is conceivable that that KA may have a pharmacological potential to reduce lipid accumulation in non-alcoholic fatty liver disease.

• Molecules and Cells
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• v.41 no.6
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• pp.603-611
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• 2018

Triglyceride homeostasis is a key process of normal development and is essential for the maintenance of energy metabolism. Dysregulation of this process leads to metabolic disorders such as obesity and hyperlipidemia. Here, we report a novel function of the Drosophila flightless-I (fliI) gene in lipid metabolism. Drosophila fliI mutants were resistant to starvation and showed increased levels of triglycerides in the fat body and intestine, whereas fliI overexpression decreased triglyceride levels. These flies suffered from metabolic stress indicated by increased levels of trehalose in hemolymph and enhanced phosphorylation of eukaryotic initiation factor 2 alpha ($eIF2{\alpha}$). Moreover, upregulation of triglycerides via a knockdown of fliI was reversed by a knockdown of desat1 in the fat body of flies. These results indicate that fliI suppresses the expression of desat1, thereby inhibiting the development of obesity; fliI may, thus, serve as a novel therapeutic target in obesity and metabolic diseases.

• Journal of Microbiology and Biotechnology
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• v.28 no.10
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• pp.1691-1699
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• 2018

A metabolically-engineered Deinococcus radiodurans R1 strain capable of producing phytoene, a colorless $C_{40}$ carotenoid and a promising antioxidant, has been developed. To make this base strain, first, the crtI gene encoding phytoene desaturase was deleted to block the conversion of phytoene to other carotenoids such as lycopene and ${\gamma}$-carotene. This engineered strain produced $0.413{\pm}0.023mg/l$ of phytoene from 10 g/l of fructose. Further enhanced production of phytoene up to $4.46{\pm}0.19mg/l$ was achieved by overexpressing the crtB gene encoding phytoene synthase and the dxs genes encoding 1-deoxy-$\text\tiny{D}$-xylulose-5-phosphate synthase gene, and by deleting the crtD gene. High cell-density culture of our final engineered strain allowed production of $10.3{\pm}0.85mg/l$ of phytoene with the yield and productivity of $1.04{\pm}0.05mg/g$ and $0.143{\pm}0.012mg/l/h$, respectively, from 10 g/l of fructose. Furthermore, the antioxidant potential of phytoene produced by the final engineered strain was confirmed by in vitro DPPH radical-scavenging assay.

• Biomedical Science Letters
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• v.24 no.4
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• pp.311-318
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• 2018

Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.

• Korean Journal of Food Science and Technology
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• v.51 no.6
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• pp.558-564
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• 2019

Hypertriglyceridemia is one of the metabolic syndrome that is often observed as a result of lipid abnormalities. It is associated with other lipids, metabolic disorders, cardiovascular disease and liver disease. Korean red ginseng is known to affect obesity, dyslipidemia, liver disease and liver function, but the mechanism of its effect is not clear. This study examined the beneficial effects of hypertriglyceridemia and the mechanism of action of Jinan red ginseng extract (JRG) in hepatoma cells. To measure the levels of triglyceride accumulation, we studied the expression of proteins and mRNAs related to lipidogenesis in hepatoma cells (Huh7 and HepG2). JRG decreases the lipidogenic markers, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding proteins α (C/EBPα) and C/EBPβ which are major regulators of triglyceride synthesis in hepatoma cells. We also found that JRG reduced sterol regulatory element binding proteins 1c (SREBP-1c), C/EBPα and C/EBPβ by regulating liver X receptor (LXR) and stearoyl CoA desaturase (SCD) expressions. In addition, the first-limited step of synthesis triglyceride (TG), glycerol-3-phosphate (G3P) is decreased by JRG. These results suggest that the anti-hypertriglyceride effect of JRG in hepatoma cells could be accompanied with the inhibition of lipidogenic transcription factors by regulating LXR and SCD expression.

• Microbiology and Biotechnology Letters
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• v.49 no.2
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• pp.210-216
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• 2021

This study aimed to enhance ethanol productivity of Saccharomyces cerevisiae through genome editing using CRISPR/CAS9. To increase ethanol productivity, ACC1, ELO1, and OLE1 were overexpressed in S. cerevisiae using the CRISPR/CAS9 system. The strains overexpressing ACC1, ELO1, and OLE1 survived up to 24 h in YPD medium supplemented with 18% ethanol. Moreover, the ethanol yields in strains overexpressing ACC1 (428.18 mg ethanol/g glucose), ELO1 (416.15 mg ethanol/g glucose), and OLE1 (430.55 mg ethanol/g glucose) were higher than those in the control strains (400.26 mg ethanol/g glucose). In conclusion, the overexpression of these genes increased the viability of S. cerevisiae at high ethanol concentrations and the ethanol productivity without suppressing glucose consumption.

• Ocean and Polar Research
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• v.44 no.1
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• pp.61-67
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• 2022

In this study, in order to evaluate the anti-obesity effect of sargassum horneri extract, the effects of the extract on lipase activity and preadipocyte differentiation in 3T3-L1 cells were investigated. S. horneri extract between 0.0 and 1.0 mg/mL showed no cytotoxicity and inhibited lipase activity by 68.1%. When S. horneri extract was utilized at levels of 0.25, 0.5, and 1.0 mg/mL in 3T3-L1 cells, preadipocytes differentiation decreased by 11.4, 19.7, and 25.6%, respectively, showing anti-obesity effects. In addition, after treatment with 1.0 mg/mL S. horneri extract, the mRNA expression levels of sterol regulatory element binding proteins-1c (SREBP-1c), peroxisome proliferator activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (CEBP-α), fatty acid synthase (FAS), and stearoyl-CoA desaturase1 (SCD1) in 3T3-L1 cells were significantly decreased (p < 0.05) by 65.2, 54.9, 50.0, 33.8, and 33.8% respectively. These results showed that S. horneri extract suppresses lipase activity and prophylactic preadipocyte differentiation in 3T3-L1, and thus can be used as an anti-obesity agent in functional foods and medicines.

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