Soo Jin Oh

Sungkyunkwan University, Sŏul, Seoul, South Korea

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Publications (52)140.74 Total impact

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    ABSTRACT: meso-Dihydroguaiaretic acid (MDGA) is a major component of Myristica fragrans and Machilus thunbergii that is traditionally used as a spice and for medicinal purposes. Despite reports of various biological activities exerted by MDGA, there is no information regarding its metabolic properties. The purpose of this study was to determine the metabolic stability and cytochrome P450 (CYP) inhibitory potential of MDGA, using pooled human liver microsomes (HLMs) to characterize its metabolic properties. In addition, pharmacokinetic analysis was performed in mice treated intravenously (5 mg/kg) or orally (20 mg/kg) with MDGA for comparison with our in vitro results. The half-life of MDGA in HLMs and mouse liver microsomes incubated with NADPH, UDPGA or NADPH plus UDPGA was 25.41 and 22.74, 0.39 and 0.20 or 0.28 and 0.22 min, respectively. In our pharmacokinetic study, MDGA rapidly declined in plasma and had low bioavailability, which was attributable to extensive metabolism by UDP-glucuronosyltransferases and CYPs. Among CYP isoforms, CYP2E1 activity was selectively inhibited by MDGA through a competitive inhibitory mode, with an inhibitory constant (Ki) value of 13.1 µM. These results suggest that MDGA can be used as a selective CYP2E1 inhibitor in vitro, which warrants evaluation of the pharmacological significance of MDGA-induced CYP2E1 inhibition. Copyright © 2014. Published by Elsevier Ltd.
    Food and Chemical Toxicology 12/2014; · 2.61 Impact Factor
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    ABSTRACT: In the present study, we investigated the combinatorial effects of betaine supplementation and boxthorn (Lycium chinense Mill.) leaf on high-fat diet (HFD)-induced body weight/body fat increase, plasma lipid profile and liver damage. Suboptimal dosage of hot water extract of boxthorn leaf (Lycium chinense water extract, LWE) exerted partial inhibitory effect on body weight/body fat increase in HFD-fed mice. Betaine supplementation potentiated the effect of LWE showing a significant inhibition against HFD-induced increase in body weight/body fat. However, both LWE alone and LWE plus betaine had no effect on plasma cholesterols, including total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol in HFD-fed mice. In contrast, HFD-induced increases in plasma and liver triglycerides were partially suppressed by LWE treatment and this was potentiated by betaine supplementation. In addition, both LWE alone and LWE plus betaine significantly suppressed HFD-induced glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase. Collectively, our results suggest that the combination of boxthorn leaf and betaine might be beneficial for the management of obesity and nonalcoholic fatty liver disease.Practical ApplicationsFor a long time, a combination of various substances was used to treat diseases effectively in traditional Chinese medicine. In the present study, we demonstrated that the supplementation of betaine synergizes with boxthorn leaf for improvement of high-fat diet-induced body weight/body fat increase and plasma/liver triglycerides accumulation. The results presented in this report suggest that the combination of boxthorn leaf and betaine might be beneficial for the treatment of obesity and related metabolic disorders.
    Journal of Food Biochemistry 12/2014; · 0.85 Impact Factor
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    ABSTRACT: In the present study, we investigated the effect of agelasine D (AD) on osteoclastogenesis. Treatment of bone marrow macrophages (BMMs) with receptor activator of nuclear factor κB ligand (RANKL) resulted in a differentiation of BMMs into osteoclasts as evidenced by generation of tartrate-resistant acid phosphatase (TRAP)-positive, multinucleated cells and formation of pits in calcium phosphate-coated plates. However, RANKL-induced osteoclastogenesis was significantly suppressed by AD treatment. We also confirmed the increased mRNA and protein expression of osteoclastic markers, such as TRAP, cathepsin K and matrix metalloproteinase-9, during RANKL-induced osteoclast differentiation and this was down-regulated by AD treatment. Moreover, AD treatment significantly suppressed RANKL-induced mRNA expression of DC-STAMP and OC-STAMP and cell fusion of TRAP-positive mononuclear osteoclast precursors. In addition, AD suppressed RANKL-induced expression of transcription factors, c-Fos and nuclear factor of activated T cells c1 (NFATc1), which are important transcription factors involved in differentiation of BMMs into osteoclasts. Furthermore, RANKL-induced phosphorylation of extracellular signal-related kinase (ERK) and activation of NF-κB were also inhibited by AD treatment. Collectively, these results suggest that AD inhibits RANKL-induced osteoclastogenesis by down-regulation of multiple signaling pathways involving c-Fos, NFATc1, NF-κB and ERK. Our results also suggest that AD might be a potential therapeutic agent for prevention and treatment of osteoporosis.
    Marine Drugs 11/2014; 12(11):5643-56. · 3.51 Impact Factor
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    ABSTRACT: Although various in vitro assays have been developed to evaluate the cytochrome P450 (CYP)-inducing potential of drug candidates, there is a continuing need for the development of a reliable model in drug discovery. The objective of the present study was to compare CYP induction by chemicals in HepG2 cells with Huh7, NKNT-3, and reverted NKNT-3 cells. HepG2 cells showed more similarity to human liver than the other cell lines in comparisons of the expression of cellular proteins. In evaluation of basal CYP activity, Huh7 cells exhibited the highest CYP1A2 and CYP3A4 activity, and HepG2 cells showed the highest CYP2B6 activity. The inducibility of CYP1A2, CYP2B6, and CYP3A4 by prototypical inducers was determined using enzyme assay, immunoblot analysis, and real-time PCR. Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4. Moreover, HepG2 cells were responsive to various CYP1A2, CYP2B6, and CYP3A4 inducers as determined using fluorogenic and LC-MS/MS substrates. Thus, HepG2 cells may be comparable to human hepatocytes for the evaluation of CYP induction or slightly less sensitive. These results suggest HepG2 cells as a cell-based model in screening for CYP inducers in drug discovery.
    Archives of Pharmacal Research 10/2014; · 1.54 Impact Factor
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    ABSTRACT: GABA is the major inhibitory transmitter in the brain and is released not only from a subset of neurons but also from glia. Although neuronal GABA is well-known to be synthesized by glutamic acid decarboxylase (GAD), the source of glial GABA is unknown. After estimating the concentration of GABA in Bergmann glia to be around 5–10 mM by immunogold electron microscopy, we demonstrate that GABA production in glia requires MAOB, a key enzyme in the putrescine degradation pathway. In cultured cerebellar glia, both Ca2+-induced and tonic GABA release is significantly reduced by both gene-silencing of MAOB and the MAOB inhibitor selegiline. In the cerebellum and striatum of adult mice, general gene-silencing, knock out of MAOB or selegiline treatment resulted in elimination of tonic GABA currents recorded from granule neurons and medium spiny neurons. Glial specific rescue of MAOB resulted in complete rescue of tonic GABA currents. Our results identify MAOB as a key synthesizing enzyme of glial GABA, which is released via Bestrophin 1 (Best1) channel to mediate tonic inhibition in the brain.This article is protected by copyright. All rights reserved
    The Journal of Physiology 09/2014; · 4.38 Impact Factor
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    ABSTRACT: 1. The herb–drug interaction potential of Hwang-Ryun-Hae-Dok-Tang (HR) extracts mediated by cytochrome P450 (CYP) inhibition was determined using human liver microsomes. 2. HR strongly inhibited CYP1A2 and moderately inhibited CYP2C19, CYP2D6, and CYP3A4 (testosterone) but not CYP2A6, CYP2B6, CYP2C8, CYP2C9, and CYP3A4 (midazolam). 3. The enzyme kinetic results suggest that CYP1A2 inhibition is competitively reversible (Ki, 13.4 ± 1.8 μg/ml), and CYP2D6 inhibition is quasi-irreversible (KI, 0.234 ± 0.138 μg/ml; kinact, 0.067 ± 0.006 min−1). 4. Fermentation using Lactobacillus acidophilus attenuated the HR-induced inhibition of CYP2D6, but not the other isoforms. 5. Neither CYP1A2 nor CYP3A4 was markedly inhibited by berberine, palmatine, and geniposide—major components in HR—and CYP2D6 was inhibited by berberine (IC50, 13.8 μg/ml) in a metabolism-dependent manner. 6. The results suggest the possibility of HR–drug interaction through inhibition of CYP—particularly CYP2D6—which may be attenuated by fermentation using L. acidophilus.
    Xenobiotica 08/2014; · 2.10 Impact Factor
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    ABSTRACT: Effects of aging on hepatic expression and activity of cytochrome P450 (CYP) isoforms were investigated in male mice aged 2, 6, 18, and 30 months. Microsomal protein, total CYP, cytochrome b5 and NADPH-dependent cytochrome P450 reductase contents in liver were fully expressed in young (2-month-old) mice. Neither Cyp1a1 nor Cyp2c was detected in any aged mice. And Cyp1a2 was maximally expressed at 2 months and decreased with age. Hepatic levels of Cyp2b10 and Cyp3a11 were decreased in 30-month-old mice. Hepatic Cyp2e1 levels were constantly maintained from 2-month to 30-month old mice. Hepatic activities of ethoxyresorufin-O-deethylase and methoxyresorufin-O-demethylase were gradually decreased after 6 months. The 30-month-old mice exhibited the lowest activity of midazolam 1'-hydroxylase. Pentoxyresorufin-O-depenthylase activity was decreased in 30-month-old mice, but not statistically significant. There were no significant differences in hepatic activities of chlorzoxazone 6-hydroxylase and midazolam 4-hydroxylase. The present study shows that increasing age, especially 30-month-old mice, leads to decrease in expression and activity of hepatic CYP isoforms, suggesting that aging mice exhibit poor hepatic drug-metabolizing capacity.
    Archives of Pharmacal Research 07/2014; · 1.54 Impact Factor
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    ABSTRACT: Numerous posterior cruciate ligament (PCL) reconstruction techniques have evolved and have revealed satisfactory outcomes; however, the optimal operative method for PCL reconstruction remains controversial.
    The American Journal of Sports Medicine 06/2014; · 4.70 Impact Factor
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    ABSTRACT: Although cytochrome P450 inhibition is the major drug-drug interaction (DDI) mechanism in clinical pharmacotherapy, DDI of a number of well-established drugs have not been investigated. Rifampicin, isoniazid, pyrazinamide and ethambutol combination therapy inhibits clearance of theophylline in patients with tuberculosis. We determined the inhibitory effects of ethambutol on the activities of nine CYP isoforms including CYP1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 and 3A4 in pooled human liver microsomes (HLM). As measured by liquid chromatography-electrospray ionization tandem mass spectrometry, ethambutol exhibited strong inhibitory potential against CYP1A2 and CYP2E1, moderate against CYP2C19 and CYP2D6 and weak against CYP2A6, CYP2C9 and CYP3A4, based on the IC50 values. The Ki value of ethambutol for CYP1A2 was 1.4μM and for CYP2E1 was 2.9μM. Inhibition of CYP1A2 and CYP2E1 was not increased by preincubation with ethambutol and β-nicotinamideadenine dinucleotide phosphate (NADPH), suggesting that the ethambutol-induced CYP inhibition may not be metabolism-dependent. Kinetic analysis showed that the inhibition of CYP1A2 and CYP2E1 by ethambutol was best fit to a competitive inhibition model. Formation of 1-methylxanthene and 1,3-dimethyluric acid from theophylline in HLM were decreased to 47% and 36%, respectively, by 3.0μM ethambutol, which is comparable its IC50 value against CYP1A2. Considering its maximal plasma concentrations of ∼10μM and long half-life of ∼22h, our findings raise the possibility that ethambutol causes significant DDIs in clinical situations with drugs with narrow therapeutic index, such as theophylline, in clinical situations.
    Toxicology Letters 06/2014; · 3.36 Impact Factor
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    ABSTRACT: Inflammation is a key regulatory process in cancer development. Prolonged exposure of breast tumor cells to inflammatory cytokines leads to epithelial-mesenchymal transition, which is the principal mechanism involved in metastasis and tumor invasion. Interleukin (IL)-1β is a major inflammatory cytokine in a variety of tumors. To date, the regulatory mechanism of IL-1β-induced cell migration and invasion has not been fully elucidated. Here, we investigated the effect of zerumbone (ZER) on IL-1β-induced cell migration and invasion in breast cancer cells. The levels of IL-8 and matrix metalloproteinase (MMP)-3 mRNA were analyzed by real-time polymerase chain reaction. The levels of secreted IL-8 and MMP-3 protein were analyzed by enzyme-linked immunosorbent assay and western blot analysis, respectively. Cell invasion and migration was detected by Boyden chamber assay. The levels of IL-8 and MMP-3 expression were significantly increased by IL-1β treatment in Hs578T and MDA-MB231 cells. On the other hand, IL-1β-induced IL-8 and MMP-3 expression was decreased by ZER. Finally, IL-1β-induced cell migration and invasion were decreased by ZER in Hs578T and MDA-MB231 cells. ZER suppresses IL-1β-induced cell migration and invasion by inhibiting IL-8 expression and MMP-3 expression in TNBC cells. ZER could be a promising therapeutic drug for treatment of triple-negative breast cancer patients. Copyright © 2014 John Wiley & Sons, Ltd.
    Phytotherapy Research 05/2014; · 2.40 Impact Factor
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    ABSTRACT: In this study, we investigated the hepatoprotective effects of aged black garlic (ABG) in rodent models of liver injury. ABG inhibited carbon tetrachloride-induced elevation of aspartate transaminase (AST) and alanine transaminase (ALT), which are markers of hepatocellular damage, in SD rats. D-galactosamineinduced hepatocellular damage was also suppressed by ABG treatment. However, ABG does not affect the elevation of alkaline phosphatase (ALP), a marker of hepatobilliary damage, in rats treated with carbon tetrachloride or D-galactosamine. We also examined the effect of ABG on high-fat diet (HFD)-induced fatty liver and subsequent liver damage. ABG had no significant effect on body weight increase and plasma lipid profile in HFD-fed mice. However, HFD-induced increase in AST and ALT, but not ALP, was significantly suppressed by ABG treatment. These results demonstrate that ABG has hepatoprotective effects and suggest that ABG supplementation might be a good adjuvant therapy for the management of liver injury.
    Toxicological research. 03/2014; 30(1):49-54.
  • Biological & Pharmaceutical Bulletin 01/2014; 37(4):707. · 1.85 Impact Factor
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    ABSTRACT: With the goal of developing soluble epoxide hydrolase (sEH) inhibitors with novel chemical structures, the sEH inhibitory activities of 30 natural compounds were evaluated using both a fluorescent substrate, 3-phenyl-cyano(6-methoxy-2-naphthalenyl)methyl ester- 2-oxiraneacetic acid, and a physiological substrate, 14,15-epoxyeicosatrienoic acid. To evaluate the selectivity of sEH inhibition, the inhibition of microsomal epoxide hydrolase (mEH), which plays a critical role in detoxification of toxic epoxides, was determined using human liver microsomes. Honokiol and β-amyrin acetate, isolated from Magnolia officinalis and Acer mandshuricum, respectively, displayed strong inhibition of sEH activity, with respective IC50 values of 0.57 μM and 3.4 μM determined using the fluorescent substrate, and 1.7 μM and 6.1 μM determined using 14,15-epoxyeicosatrienoic acid. mEH activity was decreased to 49% or 61% of control activity by 25 μM honokiol or β-amyrin acetate, respectively. These results suggest that β-amyrin acetate and honokiol exhibit sEH inhibitory activity, although their sEH selectivity should be improved.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 12/2013; · 2.99 Impact Factor
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    ABSTRACT: Diabetes mellitus and its complications have been attributed in part to oxidative stress, against which antioxidant enzymes constitute a major protective mechanism. The present study was performed to investigate the effects of early stage type 2 diabetes in the absence of obesity and liver damage on hepatic antioxidant enzyme expression and oxidative stress using 9-week-old Goto-Kakizaki (GK) rats. Hepatic total antioxidant capacity determined by total oxygen radical scavenging capacity and lipid peroxidation determined by malondialdehyde in plasma and liver were not significantly different between normal Wistar rats and GK rats. These results indicated that oxidative stress is not evident in these type 2 diabetic rats. Hepatic expression levels of antioxidant enzymes, including superoxide dismutase-1, catalase, glutathione peroxidase and reductase, thioredoxin-1, mu- and pi-class glutathione S-transferase (GST), and the gamma-glutamylcysteine ligase catalytic subunit, were not different between normal rats and GK rats. But, hepatic level and activity of alpha-class GST were decreased and peroxiredoxin-1 level was increased in GK rats, suggesting that upregulation of peroxiredoxin-1 compensates for downregulation of alpha-class GST. These results suggest that alpha-class GST and peroxiredoxin-1 in liver can be altered during the early stages of type 2 diabetes in the absence of obesity and severe oxidative stress.
    Archives of Pharmacal Research 11/2013; · 1.75 Impact Factor
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    ABSTRACT: We aimed to develop a cell culture model of type 2 diabetes by treating SK-Hep-1 cells with four free fatty acids [i.e., palmitic acid, stearic acid (SA), linoleic acid and oleic acid]. The results showed that Akt phosphorylation was increased in SK-Hep-1 cells treated with insulin in a time- and concentration-dependent manner, which was inhibited by saturated fatty acids, but not by unsaturated fatty acids. Moreover, protein levels of NADPH oxidase (NOX) 4 but not NOX2 were increased following SA treatment and, consequently, increased reactive oxygen species production and decreased cellular glutathione were observed. Apocynin, a NOX4 inhibitor, restored the SA-induced inhibition of Akt phosphorylation, suggesting the role of NOX4 in insulin resistance induced by SA. Neither phosphorylation level nor protein level of the stress signaling kinases, such as c-Jun N-terminal kinase or p38 mitogen activated protein kinase, was changed by SA treatment. Although binding immunoglobulin protein, a marker of endoplasmic reticulum stress, was transiently increased in SKHep-1 cells treated with SA, 4-phenyl butyric acid, a chemical chaperone, had no effect on the insulinmediated Akt phosphorylation inhibited by SA. The present study provides a useful model for screening anti-insulin resistance drugs and finding new drug targets for treatment of diabetes.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 11/2013; · 2.99 Impact Factor
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    ABSTRACT: The purpose of this study was to conduct a literature review of studies that have addressed rehabilitation after posterior cruciate ligament (PCL) reconstruction. In particular, we intended to perform categorical analysis and discuss some critical points. A literature review of English language articles was performed using the PubMed databases. Our literature search was performed using the following text words: [posterior cruciate ligament OR PCL] AND [reconstruction] AND [rehabilitation]. A total of 34 articles met our criteria and were included in the final systematic review. Rehabilitation protocols were reviewed and tabulated according to main rehabilitation protocol categories [range of motion (ROM), weight bearing, bracing, and strengthening]. Ranges of motion of 90° and 120° were allowed at 4-8 and 6-12 weeks postoperatively in 70 % of studies. Full weight bearing was delayed until 6 weeks postoperatively in 60 % of studies. Most studies (73 % of studies) used a brace for 6-8 weeks and active hamstring exercise was not allowed for 6-24 weeks postoperatively. The review showed that flexion of 90° was allowed at around 6 weeks and prone passive flexion exercise or supine passive ROM exercise with posterior support was used to prevent a posteriorly directed force. Most authors used non-weight bearing or partial weight bearing in their rehabilitation programs, however it may be possible to perform active weight bearing in full extension or early flexion grades as soon as the soft tissue situation allows. Co-strengthening exercises could be recommended because these exercises produce co-contraction between the quadriceps and hamstring muscles with little posterior shear force.
    Archives of Orthopaedic and Trauma Surgery 09/2013; · 1.36 Impact Factor
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    ABSTRACT: The purpose of this study was to characterize the pharmacokinetics and metabolism of 4-O-methylhonokiol in rats. The absorption and disposition of 4-O-methylhonokiol were investigated in male Sprague-Dawley rats following a single intravenous (2 mg/kg) or oral (10 mg/kg) dose. Its metabolism was studied in vitro using rat liver microsomes and cytosol. 4-O-Methylhonokiol exhibited a high systemic plasma clearance and a large volume of distribution. The oral dose gave a peak plasma concentration of 24.1±3.3 ng/mL at 2.9±1.9 h and a low estimated bioavailability. 4-O-Methylhonokiol was rapidly metabolized and converted at least in part to honokiol in a concentration-dependent manner by cytochrome P450 in rat liver microsomes, predicting a high systemic clearance consistent with the pharmacokinetic results. It was also shown to be metabolized by glucuronidation and sulfation in rat liver microsomes and cytosol, respectively. 4-O-Methylhonokiol showed a moderate permeability with no apparent vectorial transport across Caco-2 cells, suggesting that intestinal permeation process is not likely to limit its oral absorption. Taken together, these results suggest that the rapid hepatic metabolism of 4-O-methylhonokiol could be the major reason for its high systemic clearance and low oral bioavailability. Copyright © 2013 John Wiley & Sons, Ltd.
    Phytotherapy Research 07/2013; · 2.40 Impact Factor
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    ABSTRACT: In the present study, we investigated the effect of zaltoprofen enantiomers on inflammation and pain and compared their effect with racemic zaltoprofen. S(+)-zaltoprofen potently inhibited the inflammatory response in carrageenan-induced paw edema model, whereas R(-)-zaltoprofen did not. Moreover, the anti-inflammatory effect of S(+)-zaltoprofen was stronger than that of racemic zaltoprofen, suggesting that S(+)-zaltoprofen is an active component of racemic zaltoprofen in terms of anti-inflammatory activity. In contrast, the results of acetic acid-induced writhing model demonstrated that no significant analgesic effect was observed by racemic zaltoprofen and zaltoprofen enantiomers at doses used in carrageenan-induced paw edema model. However, racemic zaltoprofen and zaltoprofen enantiomers all exerted an analgesic effect at higher doses, which is inconsistent with the result of carrageenan-induced paw edema model. Gastric ulcers induced by racemic zaltoprofen and zaltoprofen enantiomers were minimal. Taken together, these results suggest that S(+)-zaltoprofen is a potent and active anti-inflammatory component of racemic zaltoprofen, but both S(+)-zaltoprofen and R(-)-zaltoprofen might seem to contribute to the analgesic effect of racemic zaltoprofen.
    International immunopharmacology 05/2013; · 2.21 Impact Factor
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    ABSTRACT: Elevated plasma homocysteine has been identified as a risk factor for cardiovascular disease and non-alcoholic liver disease, which are major complications of diabetes. Hence, hepatic homocysteine metabolism has become a major focus of diabetes research. However, little information is available regarding plasma homocysteine levels in non-obese diabetic animals. Therefore, we investigated the hepatic metabolism of sulfur-amino acids in non-obese type-2 diabetic Goto-Kakizaki rats. The experiments were performed using 9-week-old Goto-Kakizaki rats and age-matched Wistar rats. The major finding of this study is that homocysteine levels in the liver and plasma are maintained by a balance between the up-regulation of betaine homocysteine methyltransferase and the inhibition of cystathionine β-synthase in non-obese type-2 diabetic rats. Hepatic levels of cysteine and its metabolites, such as hypotaurine, taurine, and glutathione, were increased despite inhibition of the transsulfuration of homocysteine to cysteine. The elevated hepatic taurine and glutathione levels may be attributed to the up-regulation of cysteine dioxygenase expression and increased cysteine availability for glutathione synthesis. Inhibition of hepatic methionine adenosyltransferase activity in Goto-Kakizaki rats was associated with a decrease in hepatic S-adenosylmethionine, which serves as an allosteric activator of cystathionine β-synthase. The non-obese type-2 diabetic condition results in profound changes in hepatic sulfur-amino acid metabolism and raises the possibility that sulfur-amino acid metabolism may be regulated by obesity- as well as diabetes-associated factors. Further study to elucidate the pathological significance of sulfur-amino acid metabolism in chronic liver disease in type-2 diabetic animals is underway in this laboratory.
    Chemico-biological interactions 05/2013; · 2.46 Impact Factor
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    ABSTRACT: Diacylglycerol acyltransferase 2 (DGAT2) is one of two distinct DGAT enzymes that catalyze the last step in triacylglycerol (TG) synthesis. Findings from previous studies suggest that inhibition of DGAT2 is a promising strategy for the treatment of hepatic steatosis and insulin resistance. Here, we identified compound 122 as a potent and selective inhibitor of human DGAT2, which appeared to act competitively against oleoyl-CoA in vitro. The selective inhibition of DGAT2 was also confirmed by the reductions in enzymatic activity and de novo TG synthesis in DGAT2-overexpressing HEK293 cells and hepatic cells HepG2. Compound 122, as a newly identified inhibitor of DGAT2, will be useful for the research on DGAT2-related lipid metabolism as well as the development of therapeutic drug for several metabolic diseases.
    Biological & Pharmaceutical Bulletin 04/2013; · 1.85 Impact Factor

Publication Stats

235 Citations
140.74 Total Impact Points


  • 2014
    • Sungkyunkwan University
      • Samsung Medical Center
      Sŏul, Seoul, South Korea
  • 2009–2014
    • Inje University
      Kŭmhae, South Gyeongsang, South Korea
    • Inje University Paik Hospital
      Sŏul, Seoul, South Korea
  • 2010–2013
    • Korea Research Institute of Bioscience and Biotechnology KRIBB
      • Bioevaluation Center
      Anzan, Gyeonggi Province, South Korea
    • Seoul National University
      • College of Pharmacy
      Sŏul, Seoul, South Korea
  • 2006–2013
    • Chungnam National University
      • College of Pharmacy
      Sŏngnam, Gyeonggi Province, South Korea
  • 2011
    • Seoul National University of Science and Technology
      Sŏul, Seoul, South Korea
  • 2006–2010
    • Chosun University
      • College of Pharmacy
      Kwangju, Gwangju, South Korea