• Journal of Nutrition and Health
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• v.31 no.7
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• pp.1112-1120
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• 1998

This study was conducted to investigate the effets of chitosan and beef tallow at different level on glucose and lipid metabolism in rats. Dietary fot level was 20% and 40%, and chitosan was given at levels of 0%, 3%, and 5%(wt/wt) of diet. Chitosan supplement tended to decrease the serum total lipids, total cholesterol, and triglycerides. HDL cholesterol and HDL cholesterol : total cholesterol ratio tended to increase with 5% chitosan supplementation. LDL cholesterol and VLDL triglyceride tended to decrease with chitosan supplementation. Lipid concentration of liver and epididymal fat pad(EEP) tended to decrease with medium dietary fat and chitosan treatment. fecal excretion of total lipid and triglyceride exhibited a tendency to increase with high fat levels and chitosan. Length of small intestine and gastrointestinal transit time were not affected by dietary fit levels or chitosan supplements. Therefore, it could be suggested that chitosan supplement had beneficial effects on lipid metabolism. (Korean J Nutrition 31(7) : 1112-1120, 1998)

• Molecules and Cells
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• v.41 no.1
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• pp.11-17
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• 2018

Autophagy is critical for the maintenance of organelle function and intracellular nutrient environment. Autophagy is also involved in systemic metabolic homeostasis, and its dysregulation can lead to or accelerate the development of metabolic disorders. While the role of autophagy in the global metabolism of model organisms has been investigated mostly using site-specific genetic knockout technology, the impact of dysregulated autophagy on systemic metabolism has been unclear. Here, we review recent papers showing the role of autophagy in systemic metabolism and in the development of metabolic disorders. Also included are data suggesting the role of autophagy in human-type diabetes, which are different in several key aspects from murine models of diabetes. The results shown here support the view that autophagy modulation could be a new modality for the treatment of metabolic syndrome associated with lipid overload and human-type diabetes.

• Proceedings of the Korean Society of Crop Science Conference
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• 2006.04a
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• pp.602-603
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• 2006

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.19-28
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• 2018

Rapidly proliferating cancer cells require energy and cellular building blocks for their growth and ability to maintain redox balance. Many studies have focused on understanding how cancer cells adapt their nutrient metabolism to meet the high demand of anabolism required for proliferation and maintaining redox balance. Glutamine, the most abundant amino acid in plasma, is a well-known nutrient used by cancer cells to increase proliferation as well as survival under metabolic stress conditions. In this review, we provide an overview of the role of glutamine metabolism in cancer cell survival and growth and highlight the mechanisms by which glutamine metabolism affects cancer cell signaling. Furthermore, we summarize the potential therapeutic approaches of targeting glutamine metabolism for the treatment of numerous types of cancer.

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.69-80
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• 2018

Cancer cells reprogram cellular metabolism to support the malignant features of tumors, such as rapid growth and proliferation. The cancer promoting effects of metabolic reprogramming are found in many aspects: generating additional energy, providing more anabolic molecules for biosynthesis, and rebalancing cellular redox states in cancer cells. Metabolic pathways are considered the pipelines to supply metabolic cofactors of epigenetic modifiers. In this regard, cancer metabolism, whereby cellular metabolite levels are greatly altered compared to normal levels, is closely associated with cancer epigenetics, which is implicated in many stages of tumorigenesis. In this review, we provide an overview of cancer metabolism and its involvement in epigenetic modifications and suggest that the metabolic adaptation leading to epigenetic changes in cancer cells is an important non-genetic factor for tumor progression, which cooperates with genetic causes. Understanding the interaction of metabolic reprogramming with epigenetics in cancers may help to develop novel or highly improved therapeutic strategies that target cancer metabolism.

• 한국약용작물학회:학술대회논문집
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• 2009.05a
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• pp.253-254
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• 2009

• Toxicological Research
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• v.31 no.1
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• pp.25-32
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• 2015

The objectives of this study were to investigate the individual characteristics, lifestyle habits, exposure levels, and genetic diversity of xenobiotic-metabolizing enzymes involved in toluene metabolism in Korean and foreign workers exposed to toluene at a manufacturing plant. This study was conducted to determine the effects of culture or ethnicity on toluene metabolism. The results showed that blood and urinary toluene concentrations were dependent on the level of exposure to toluene. We analyzed the correlation between toluene metabolism and genetic diversity in glutathione S-transferase (GST) (M1), GSTT1, and cytochrome p-450 (CYP) $2E1^*5$ as well as lifestyle habits (smoking, drinking, and exercise habits). The results revealed significant correlations between toluene metabolism and GSTM1 and GSTT1 genetic diversity, as well as smoking and exercise.

• Toxicological Research
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• v.31 no.2
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• pp.137-149
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• 2015

Human hepatocytes, with complete hepatic metabolizing enzymes, transporters and cofactors, represent the gold standard for in vitro evaluation of drug metabolism, drug-drug interactions, and hepatotoxicity. Successful cryopreservation of human hepatocytes enables this experimental system to be used routinely. The use of human hepatocytes to evaluate two major adverse drug properties: drug-drug interactions and hepatotoxicity, are summarized in this review. The application of human hepatocytes in metabolism-based drug-drug interaction includes metabolite profiling, pathway identification, P450 inhibition, P450 induction, and uptake and efflux transporter inhibition. The application of human hepatocytes in toxicity evaluation includes in vitro hepatotoxicity and metabolism-based drug toxicity determination. A novel system, the Integrated Discrete Multiple Organ Co-culture (IdMOC) which allows the evaluation of nonhepatic toxicity in the presence of hepatic metabolism, is described.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.13 no.1
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• pp.20-29
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• 2013

Inborn error of metabolism usually presents with a constellation of clinical pictures involving multiorgan systems. Because of its rarity and clinical diversity, it is difficult to make diagnosis accurately and efficiently. Many inborn error of metabolism shows predominantly hepatic symptoms and signs. The onset of symptoms is also varying depending the disease. The onset might be even prenatal, either neonatal or infantile, and late childhood. The major manifestation patterns are jaundice or cholestasis, hepatomegaly with or without splenomegaly, hypoglycemia and acute or chronic hepatocellular dysfunction. Based on pronounced hepatic symptoms and onset of symptoms, differential diagnosis can be more easily made with subsequent further laboratory investigation. In this review paper, major inborn error of metabolism with hepatic symptoms are described from the perspective of mode of clinical presentations.

• Journal of Food Hygiene and Safety
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• v.11 no.1
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• pp.31-34
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• 1996

Aloe, being used widely as a health food and also as a traditional folk remedy for burns and constipation, contains quinone derivatives particularly in its skin. Thus, we have investigated the effect of extracts of Aloe in ethanol metabolism. The dried powder of water extract of skinned Aloe (300 mg/kg body weight given to rats by oral adminstration at 30 min prior to oral adminstration of ethanol given at a does of 4 gm/kg) and the freeze-dried Aloe gel commercial product (600 mg/kg) which was prepared after selective elimination of quinones were found not to increase the ethanol metabolism rate in vivo. This result suggested that quinones, missing from the above preparations, might be responsible for enhancing ethanol metabolism rate.