Chinju, South Korea
Chinju, South Korea

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Jung U.J.,Pukyong National University | Cho Y.-Y.,Amicogen Inc. | Choi M.-S.,Kyungpook National University
Nutrients | Year: 2016

Several in vitro and in vivo studies have reported the anti-inflammatory, anti-diabetic and anti-obesity effects of the flavonoid apigenin. However, the long-term supplementary effects of low-dose apigenin on obesity are unclear. Therefore, we investigated the protective effects of apigenin against obesity and related metabolic disturbances by exploring the metabolic and transcriptional responses in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed an HFD or apigenin (0.005%, w/w)-supplemented HFD for 16 weeks. In HFD-fed mice, apigenin lowered plasma levels of free fatty acid, total cholesterol, apolipoprotein B and hepatic dysfunction markers and ameliorated hepatic steatosis and hepatomegaly, without altering food intake and adiposity. These effects were partly attributed to upregulated expression of genes regulating fatty acid oxidation, tricarboxylic acid cycle, oxidative phosphorylation, electron transport chain and cholesterol homeostasis, downregulated expression of lipolytic and lipogenic genes and decreased activities of enzymes responsible for triglyceride and cholesterol ester synthesis in the liver. Moreover, apigenin lowered plasma levels of pro-inflammatory mediators and fasting blood glucose. The anti-hyperglycemic effect of apigenin appeared to be related to decreased insulin resistance, hyperinsulinemia and hepatic gluconeogenic enzymes activities. Thus, apigenin can ameliorate HFD-induced comorbidities via metabolic and transcriptional modulations in the liver. © 2016 by the authors; licensee MDPI, Basel, Switzerland.


Park H.J.,Kyungpook National University | Lee M.K.,Sunchon National University | Park Y.B.,Kyungpook National University | Shin Y.C.,Amicogen Inc. | Choi M.S.,Kyungpook National University
Food and Chemical Toxicology | Year: 2011

This study was performed to evaluate the beneficial effect of Undaria pinnatifida ethanol extract (UEFx) on insulin resistance in diet-induced obese mice. A high-fat diet was supplemented with the UEFx at 0.69% (wt/wt) dose, which contains an equivalent amount of 0.02% fucoxanthin (wt/wt), or with Fx at 0.02% (wt/wt) dose in diet. After 9 weeks, both UEFx supplement significantly lowered the amount of visceral fat, the size of adipocyte, the fasting blood glucose concentration, the plasma insulin and the insulin resistance index similar to pure as shown by Fx supplement, compared to the high-fat (HF) control group. Blood glucose level was negatively correlated with hepatic glucokinase activity (r= -0.533, p< 0.05), whereas positively correlated with hepatic gluconeogenic enzyme activities (r= 0.463, p< 0.05 for glucose-6-phosphatase; r= 0.457, p< 0.05 for phosphoenolpyruvate carboxykinase). Ratio of hepatic glucokinase/glucose-6-phosphatase and glycogen content were significantly elevated by the UEFx and Fx supplements. Supplementation of the UEFx as well as Fx seemed to stimulate the β-oxidation activity and inhibit the phosphatidate phosphohydrolase activity resulting in a decrease in the hepatic lipid droplet accumulation. The results indicate that the UEFx can prevent insulin resistance and hepatic fat accumulation that is partly mediated by modulating the hepatic glucose and lipid homeostasis in the high fat-induced obese mice. © 2010 Elsevier Ltd.


Woo M.-N.,Kyungpook National University | Jeon S.-M.,Kyungpook National University | Kim H.-J.,CJ CheilJedang Corporation | Lee M.-K.,Sunchon National University | And 4 more authors.
Chemico-Biological Interactions | Year: 2010

This study investigated the effects of fucoxanthin isolated from marine plant extracts on lipid metabolism and blood glucose concentration in high-fat diet fed C57BL/6N mice. The mice were divided into high-fat control (HFC; 20% fat, w/w), low-fucoxanthin (low-Fxn; HFC+0.05% Fxn, w/w) and high-fucoxanthin (high-Fxn; HFC+0.2% Fxn, w/w) groups. Fxn supplementation significantly lowered the concentration of plasma triglyceride with a concomitant increase of fecal lipids in comparison to the HFC group. Also, the hepatic lipid contents were significantly lowered in the Fxn supplemented groups which seemed to be due to the reduced activity of the hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase, malic enzyme, fatty acid synthase and phosphatidate phosphohydrolase and the enhanced activity of β-oxidation. Plasma high-density lipoprotein cholesterol concentrations and its percentage were markedly elevated by Fxn supplementation. Activities of two key cholesterol regulating enzymes: 3-hydroxy-3-methylglutaryl coenzyme A reductase and acyl coenzyme A: cholesterol acyltransferase, were significantly suppressed by Fxn regardless of the dosage. Relative mRNA expressions of acyl-coA oxidase 1, palmitoyl (ACOX1) and peroxisome proliferators activated receptor α (PPARα) and γ (PPARγ) were significantly altered by Fxn supplementation in the liver. Fxn also lowered blood glucose and HbA1c levels along with plasma resistin and insulin concentrations. These results suggest that Fxn supplementation plays a beneficial role in not only regulating the plasma and hepatic lipids metabolism but also for blood glucose-lowering action in high-fat fed mice. © 2010 Elsevier Ireland Ltd.


PubMed | Pukyong National University, Kyungpook National University and Amicogen Inc.
Type: Journal Article | Journal: Nutrients | Year: 2016

Several in vitro and in vivo studies have reported the anti-inflammatory, anti-diabetic and anti-obesity effects of the flavonoid apigenin. However, the long-term supplementary effects of low-dose apigenin on obesity are unclear. Therefore, we investigated the protective effects of apigenin against obesity and related metabolic disturbances by exploring the metabolic and transcriptional responses in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed an HFD or apigenin (0.005%, w/w)-supplemented HFD for 16 weeks. In HFD-fed mice, apigenin lowered plasma levels of free fatty acid, total cholesterol, apolipoprotein B and hepatic dysfunction markers and ameliorated hepatic steatosis and hepatomegaly, without altering food intake and adiposity. These effects were partly attributed to upregulated expression of genes regulating fatty acid oxidation, tricarboxylic acid cycle, oxidative phosphorylation, electron transport chain and cholesterol homeostasis, downregulated expression of lipolytic and lipogenic genes and decreased activities of enzymes responsible for triglyceride and cholesterol ester synthesis in the liver. Moreover, apigenin lowered plasma levels of pro-inflammatory mediators and fasting blood glucose. The anti-hyperglycemic effect of apigenin appeared to be related to decreased insulin resistance, hyperinsulinemia and hepatic gluconeogenic enzymes activities. Thus, apigenin can ameliorate HFD-induced comorbidities via metabolic and transcriptional modulations in the liver.


Sontakke S.B.,Gyeongsang National University | Jung J.-H.,Amicogen Inc. | Piao Z.,Amicogen Inc. | Chung H.J.,Gyeongsang National University
Journal of Agricultural and Food Chemistry | Year: 2016

Collagen-derived small peptides, such as Gly-Pro-Hyp (GPH) and Pro-Hyp (PH), play a role in various physiological functions. Although collagen degrades in the gastrointestinal tract randomly and easily, it is not readily cleaved into bioactive peptides. To increase the bioavailability of bioactive peptides, a collagen tripeptide (CTP) was prepared from fish scales by the digestion method using collagenase from nonpathogenic Bacillus bacteria. It was demonstrated that Hyp-containing peptides - GPH and PH - were better absorbed and reached higher plasma levels after the oral administration of CTPs in rats compared to high molecular weight collagen peptide (H-CP). GPH and PH were stable in gastrointestinal fluid and rat plasma for 2 h, and GPH was able to be transported across the intestinal cell monolayer. These results suggest that the ingestion of CTP is an efficient method for taking bioactive peptides orally due to the enzymatic stability and intestinal permeability of GPH and PH. © 2016 American Chemical Society.


Hwang Y.P.,Chungnam National University | Kim H.G.,Chungnam National University | Han E.H.,Chungnam National University | Choi J.H.,Chungnam National University | And 4 more authors.
Journal of Dermatological Science | Year: 2011

Background: N-Acetylglucosamine (GlcNAc) and its derivates have been utilized in dietary supplements and for therapeutic development due to their unique characteristics. GlcNAc is recognized primarily for its function as a precursor to hyaluronic acid, which plays a significant role in the structure and hydration of the extracellular matrix in skin, in both the epidermis and the dermis. Objective: We investigated the protective effects of GlcNAc on immortalized human skin fibroblasts (HS68) against UVB damage. We then explored the inhibitory effects of GlcNAc on UVB-induced collagenases and investigated the molecular mechanism underlying those effects. Methods: Those effects were assessed by semi-quantitative PCR, Western blotting and enzymatic activity assays. Results: GlcNAc increased the viability of, and inhibited ROS production in, HS68 cells exposed to UVB irradiation. Pre-treatment of HS68 cells with GlcNAc inhibited UVB-induced production of the collagenases MMP-1 and MMP-13. Western blot analysis further revealed that GlcNAc markedly suppressed the enhancement of collagen degradation in UVB-exposed HS68 cells. GlcNAc also suppressed UVB-induced activation of c-Jun, c-Fos and NF-κB and the phosphorylation of MAPKs and PI3K/Akt, upstream modulators of AP-1 and NF-κB. Moreover, GlcNAc decreased the UVB-induced influx of Ca2+ into HS68 cells and the phosphorylation of Ca2+/calmodulin-dependent kinases (CaMKs). Conclusion: The results indicate that GlcNAc inhibited UVB-induced collagenolytic MMP production by interfering with Ca2+-dependent Akt and MAPKs/AP-1 and NF-κB signaling. They may thus be potentially useful in the prevention and treatment of skin photoaging. © 2011 Japanese Society for Investigative Dermatology.


Choi G.N.,Gyeongsang National University | Kim J.H.,Gyeongsang National University | Kim J.H.,Korea forest Research Institute | Kwak J.H.,Gyeongsang National University | And 5 more authors.
Food Chemistry | Year: 2012

To investigate the anti-amnesic effect of quercetin by using in vivo Y-maze and passive avoidance tests, the learning and memory impairment in ICR mice was induced by neurotoxic trimethyltin. Quercetin pre-administration attenuated TMT-induced memory injury in both in vivo tests. Acetylcholinesterase (AChE), prepared from mice brain tissues, was inhibited by quercetin in a dose-dependent manner. Malondialdehyde generation in the brain homogenate of mice treated with quercetin decreased, indicating that peroxidation of polyunsaturated fatty acids was inhibited by the cellular membrane. In addition, potent antioxidant capacity of quercetin was confirmed through various antioxidative assays. Our findings suggest that the quercetin may improve cognitive ability against TMT-induced neuronal deficit and also have an inhibitory action against AChE. Consequently, these results demonstrate that the quercetin could possess a wide range of beneficial activities for neurodegenerative disorders, notably Alzheimer's disease (AD). © 2011 Elsevier Ltd. All rights reserved.


PubMed | Gyeongsang National University, Ewha Womans University, Konkuk University, Amicogen Inc. and Sunchon National University
Type: Journal Article | Journal: Archives of pharmacal research | Year: 2016

-N-acetylglucosamine (-AG) is a monosaccharide distributed widely in living organisms with various pivotal roles. The presence of particulates and impurities can affect the safety and efficacy of a product for its intended duration of use. Thus, the current study was carried out to identify and quantify the potentially-harmful process related impurities; namely -N,6-diacetylglucosamine (-DAG) and -N-acetylglucosamine (-AG), derived from the chemical and enzymatic synthesis of -AG. The impurities were characterized using a high resolution mass spectrometry, a nuclear magnetic resonance spectroscopy, and liquid chromatography-tandem mass spectrometry (LC/MS/MS). The developed method showed a good linearity (R (2)0.998), satisfactory precision (6.1% relative standard deviation), intra- and inter-day accuracy (88.20-97.50%), extraction recovery (89.30-110.50%), matrix effect (89.70-105.20%), and stability (92.70-101.60%). The method was successfully applied to determine the level of -DAG that was 3.04 and 0.07% of the total -AG, following chemical and enzymatic methods, respectively. It can be concluded that the enzymatic rather than the chemical method is more efficient for the synthesis of -AG. Characterization of impurities heeds the signal for acquiring and evaluating data that establishes biological safety.


PubMed | Wenzhou University, Amicogen Inc. and Zhejiang University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Fibroblast growth factor (FGF)21 functions in the maintenance of glucose homeostasis and exerts protective effects on the liver, heat and kidneys. However, the roles of FGF21 in other tissue types are yet to be fully elucidated. The present study detected elevated expression levels of FGF21 in skin tissue. Furthermore, it was revealed that FGF21 expression in the skin was induced upon wounding. In addition, klotho expression was detected in the skin tissue. To examine the role of FGF21 in the wound healing process, recombinant human (h)FGF21 was expressed in a the yeast strain Pichia (P.) pastoris, a wellknown system for recombinant protein production. Based on the sequence of hFGF21 and the optimal codon of P. pastoris, codonoptimized FGF21 open reading frame sequences were obtained using seven pairs of 5559nt primers with seven rounds of PCR. The recombinant FGF21 was purified and its function was examined in human fibroblast cells using a wound healing cell migration assay. Treatment with FGF21 promoted cell migration, which is an important step in wound healing. Furthermore, FGF21 treatment enhanced the activity of cJun Nterminal kinase, a key regulator in fibroblastcell migration. In conclusion, FGF21 is induced after wounding and FGF21 expressed and purified from yeast markedly accelerates wound healing. The present study was the first to elucidate the function of FGF21 in skin tissues and provided a theoretical basis for the use of FGF21 in the treatment of skin wounds.


Patent
Amicogen Inc. | Date: 2012-06-28

A method of producing lycopene, with high productivity by means of a recombinant bacterial strain includes preparing the recombinant vector containing genes encoding proteins, which are required for lycopene biosynthesis. The genes involved in lycopene biosynthesis are crtE, crtB and crtI, and at least one of the said three genes (crtE, crtB and crtI) is selected from the group consisting of crtE with the SEQ ID NO:1, crtB with the SEQ ID NO:3 and crtI with the SEQ ID NO:5, of the Sequence List. The said recombinant vector is transformed into Escherichia coli (hereafter E. coli). The E. coli transformant is cultured to recover lycopene from the culture medium.

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