• The Journal of Korean Medicine
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• v.38 no.1
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• pp.72-80
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• 2017

Objectives: The purpose of this study is to evaluate the urinary organic acid comprehensive profile for chemotherapy induced peripheral neuropathy (CIPN). Methods: Participants are 66 patients with CIPN who had symptom (Visual analog scale ${\geq}30mm$, Eastern Cooperative Oncology Group ${\leq}2$). Participants were tested with organic acid comprehensive profile markers. Results: Positive Correlation was observed in the neurotransmitter metabolism markers, N-methyl-D-aspartate (NMDA) modulators markers, detoxification markers, energy production markers, amino acid metabolism markers, and intestinal dysbiosis markers. Especially, all the neurotransmitter metabolism markers were showed positive rate of 44%. In addition, neuro-endo-immune was associated with energy metabolism (mitochondrial dysfunction) in CIPN of cancer patient. especially detoxification, intestinal bacterial hyperplasia, vitamin deficiency (folate, complex B group, vitamin C). Conclusions: Significant urinary organic acid comprehensive profile results were obtained in cancer patients who induced peripheral neuropathy by chemotherapy.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.45-54
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• 2017

Our study aims to determine the metabolism and excretion of novel pulmonary-targeting docetaxel liposome (DTX-LP) using the in vitro and in vivo animal experimental models. The metabolism and excretion of DTX-LP and intravenous DTX (DTX-IN) in New Zealand rabbits were determined with ultra-performance liquid chromatography tandem mass spectrometry. We found DTX-LP and DTX-IN were similarly degraded in vitro by liver homogenates and microsomes, but not metabolized by lung homogenates. Ultra-performance liquid chromatography tandem mass spectrometry identified two shared DTX metabolites. The unconfirmed metabolite $M_{un}$ differed structurally from all DTX metabolites identified to date. DTX-LP likewise had a similar in vivo metabolism to DTX-IN. Conversely, DTX-LP showed significantly diminished excretion in rabbit feces or urine, approximately halving the cumulative excretion rates compared to DTX-IN. Liposomal delivery of DTX did not alter the in vitro or in vivo drug metabolism. Delayed excretion of pulmonary-targeting DTX-LP may greatly enhance the therapeutic efficacy and reduce the systemic toxicity in the chemotherapy of non-small cell lung cancer. The identification of $M_{un}$ may further suggest an alternative species-specific metabolic pathway.

• Proceedings of the Ginseng society Conference
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• 1987.06a
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• pp.47-58
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• 1987

Ethanol exerts different effects on hepatic cellular metabolism, depending mainly on the duration of its intake. In the presence of ethanol following an acute load, a number of hepatic functions are inhibited, including lipid oxidation and microsomal drug metabolism. In its early stages, chronic ethanol consumption produces adaptive metabolic changes in the endoplasmic reticulum which result in increased metabolism of ethanol and drugs and accelerated lipoprotein production. Prolongation of ethanol intake may result in injurious hepatic lesions such as alcoholic hepatitis and cirrhosis A number of such metabolic effects of ethanol are directly linked to the two major products of its oxidation; hydrogen and acetaldehyde. The excess hydrogen from ethanol unbalances the liver cell's chemistry. In the presence of excess hydrogen ions the process is turned in a different direction. In this study, it was attempted to observe the effect of ginseng saponins on alcohol Oehydrogenase(ADH), aldehyde dehydrogenase(ALDH) and microsomal ethanol oxidizing system(MEOS) in vivo as well as in vitro. Furthermore, the effect of ginseng saponin on the hydrogen balance in the liver and the hepatic cellular distribution of (1-14C) ethanol, its incorporation into acetaldehyde and lipids was also investigated. It seemed that ginseng saponin stimulated the above enzymes and other related enzymes in ethanol metabolism, resulting in a rapid removal of acetaldehyde and excess hydrogen from the animal body,

• Biomolecules & Therapeutics
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• v.26 no.1
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• pp.10-18
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• 2018

Tumors are dynamic metabolic systems which highly augmented metabolic fluxes and nutrient needs to support cellular proliferation and physiological function. For many years, a central hallmark of tumor metabolism has emphasized a uniformly elevated aerobic glycolysis as a critical feature of tumorigenecity. This led to extensive efforts of targeting glycolysis in human cancers. However, clinical attempts to target glycolysis and glucose metabolism have proven to be challenging. Recent advancements revealing a high degree of metabolic heterogeneity and plasticity embedded among various human cancers may paint a new picture of metabolic targeting for cancer therapies with a renewed interest in glucose metabolism. In this review, we will discuss diverse oncogenic and molecular alterations that drive distinct and heterogeneous glucose metabolism in cancers. We will also discuss a new perspective on how aberrantly altered glycolysis in response to oncogenic signaling is further influenced and remodeled by dynamic metabolic interaction with surrounding tumor-associated stromal cells.

• BMB Reports
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• v.35 no.3
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• pp.283-290
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• 2002

The glycogen-associated protein phosphatase (PP1G/$R_{GL}$) may play a central role in the hormonal control of glycogen metabolism in the skeletal muscle. Here, we investigated the in vivo epinephrine effect of glycogen metabolism in the skeletal muscle of the wild-type and $R_{GL}$ knockout mice. The administration of epinephrine increased blood glucose levels from 200±20 to 325±20 mg/dl in both wild-type and knockout mice. Epinephrine decreased the glycogen synthase -/+ G6P ratio from 0.24±0.04 to 0.10±0.02 in the wild-type, and from 0.17±0.02 to 0.06±0.01 in the knockout mice. Conversely, the glycogen phosphorylase activity ratio increased from 0.21±0.04 to 0.65±0.07 and from 0.30±0.04 to 0.81±0.06 in the epinephrine trated wild-type and knockout mice respectively. The glycogen content of the knockout mice was substantially lower (27%) than that of both wild-type mice; and epinephrine decreased glycogen content in the wild-type and knockout mice. Also, in Western blot analysis there was no compensation of the other glycogen targeting components PTG/R5 and R6 in the knockout mice compared with the wild-type. Therefore, $R_{GL}$ is not required for the epinephrine stimulation of glycogen metabolism, and rather another phosphatase and/or regulatory subunit appears to be involved.

• Journal of Nutrition and Health
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• v.32 no.4
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• pp.376-383
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• 1999

The effects of $\beta$-carotene substitutionl for vitamin A and the chronic consumption of ethanol of ethanol on hepatic folate metabolism were studied it rats. The substitution of $\beta$-carotene for vitamin A depressed hepatic 10-formyl-tetreahydrofolate dehydrogenase(10-formyl-tetrahydrofolate : NADP oxidoreductase, E.C. 1.5. 1.6)activity to 65% of controls(p<0.001) and enhanced hepatic 5, 10-methy-lenetetrahydrofolate reductase(E. C. 6.3.3.2)activity by 56% with respect to control levels(p<0.001). Hepatic activity of 10-formyltertrahydrofolate dehydrogenase was depressed to about half that of control levels by ethanol administration to rats(36% ethanol diet, p<0.001). The activity of 5, 10-methyleneterahydrofolate reductase was not changed by ethanol consumption. The increased activity of 5, 10-methyleneterahydrofolate reductase and the decreased activity of 10-formyltetrahydrofolate dehydrogenase appeared to decrease the level of nonmethyl folate conezyme and the rate of one-carbon metabolism. Plasma homocysteine concentrations were significantly higher in rats fed ethanol(p<0.01) o $\beta$-carotene(p<0.001) than in controls, which suggests that increased activity of 5, 10-methylenetetrahydrofolate reductase can depress homocysteine metabolism. We concluded that dietary substitution of $\beta$-carotene for vitamin A or chronic administration of ethanol resulted in changes in the activity of hepatic folate-dependent enzymes, which could affect the distribution of folate derivatives, plasma homocysteine levels and one-carbon metabolism.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.3
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• pp.480-487
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• 1997

The present study was designed to examine how Ca intake contributes to the increase of peak bone mass with growing female rats. Weaned rats were fed experimental diets consisting in five levels of Ca; very low(0.1%), low(0.2%), moderate(0.5%), high(1.0%) and very high(1.5%) for 4, 8 and 12 weeks. Bone growth, metabolism and Ca metabolism were determined. As for the rats fed for 4 weeks, the bone weight, length and breaking force and bone metabolism were not significantly affected by dietary Ca levels, whereas the current intakes of Ca were observed to have significantly affected the rats fed for 8 or 12 weeks with regard to the bone weight, length and breaking force and bone metabolism. The bone ash and Ca contents of the rats were affected by dietary Ca levels for the total period of feeding. It is suggested that dietary Ca itself affected the mineralization process either during the growth or later, although the resulting bone mass is not a linear function of dietary Ca content.

• BMB Reports
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• v.42 no.3
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• pp.125-130
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• 2009

Recent advances in RNA biology reveal unexpected diversity and complexity of cellular RNA metabolism. RNA-binding proteins (RBPs) are essential players in RNA metabolism, regulating RNA splicing, transport, surveillance, decay and translation. Aberrant expression of RBPs affects many steps of RNA metabolism, significantly altering expression of RNA. Thus, altered expression and dysfuncting of RBPs are implicated in the development of various diseases including cancer. In this minireview, we briefly describe emerging roles of RBPs as a global coordinator of post-transcriptional steps and altered RBP as a global generator of cancer related RNA alternative splicing. Identification and characterization of the RNA-RBP network would expand the scope of cellular RNA metabolism and provide novel anti-cancer therapeutic targets based on cancer specific RNA-RBP interaction.

• Biomolecules & Therapeutics
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• v.20 no.5
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.

• Journal of Applied Biological Chemistry
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• v.51 no.4
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• pp.165-168
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• 2008

A processed Aconiti tuber (Korean name, Kyeong-Po Buja) was extracted with 80% aqueous EtOH, and the concentrated extract was partitioned with EtOAc and water ($H_2O$). From the EtOAc fraction, two flavonoids were isolated through repeated silica gel column chromatographies. From the result of physico-chemical data including NMR, mass spectrometry and IR, the chemical structures of the compounds were determined to be liquiritin (1) and liquiritigenin (2). This is the first study to isolate flavonoids (1) and (2) from the processed Aconiti tuber.