• Bulletin of Food Technology
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• v.7 no.2
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• pp.129-133
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• 1994

• Proceedings of the Korean Nutrition Society Conference
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• 2000.11a
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• pp.66-66
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• 2000

• Applied Biological Chemistry
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• v.42 no.1
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• pp.29-33
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• 1999

To investigate the effects of Angelica gigas Nakai diet on lipid metabolism, alcohol metabolism and liver function of rats administered with chronic ethanol, Sprague-Dawley male rats were fed either AIN-76 diet (control), control diet with ethanol, control plus Angelica gigas Nakai diet, or control plus Angelica gigas Nakai diet with ethanol for 30 days. On the 21st day, all of the rats were given an oral dose of ethanol and blood-ethanol concentration was monitored for the next 5 hours. The results obtained were: 1) Upon ethanol administration, the blood ethanol concentration was decreased from 2 hr significantly in the group of control plus Angelica gigas Nakai diet compared with control diet group; 2) The blood ethanol oxidation rate was increased in the group of control plus Angelica gigas Nakai diet with ethanol compared with control diet group or control plus Angelica gigas Nakai diet group. After 30 days, rats were sacrificed and then lipid and enzyme determinations in blood and liver were carried out. The results obtained were: 1) LDL-cholesterol in the blood of control plus Angelica gigas Nakai diet group was decreased significantly compared with control diet group; 2) Angelica gigas Nakai diet decreased liver triglyceride and total lipid and blood ${\gamma}-GTP$ level increased due to the chronic ethanol administration. These data suggest that Angelica gigas Nakai can have a recovery function on the symptoms of alcohol related diseases.

• Journal of Life Science
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• v.4 no.3
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• pp.102-112
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• 1994

알콜성 간장해의 발생, 진전에는 많은 인자가 관여하고 있으며 극히 복잡한 병태를 형성하는데 그 기전으로는 1)간내 [NADH]/[NAD] 비의 상승, 2)에탄올의 주 대사산물인 아세트알데히드에 의한 간장해, 3)면역기구에 의한 간장해, 4)과산화지질, 활성산소 및 free radical 에 의한 장해와 5) 중심정맥역의 hypoxia에 의한 간세포장해 기전을 들 수 있다. 본 총설에서는 알콜을 장기 섭취할 경우 간에서의 대사경로와 현재 고려되고 있는 몇 가지 알콜성 간장해 발생기전에 대한 최근의 연구들을 정리하였다.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.91-91
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• 1995

에탄올에 의한 급성독성은 에탄올, 아세트알데히드 및 에탄을 대사산물의 변형생성물질 등에 기인하므로 알콜 섭취 후 혈중 에탄을 농도 및 아세트알데히드의 농도를 낮추는 것은 음주에 의한 급성 중독상태에 머무는 시간을 단축시키는데 중요하다. 본 실험에서는 Bacillus subtilis natto sp.를 식물 추출액을 배지로 하여 배양한 후 단백 분해효소로 고분자물질을 절단하여 얻은 발효액인 바이오짐(상품명: Biozyme)을 주성분으로 한 '비지니스(조선무약합자회사)' 의 인체 혈중 알콜대사 촉진작용을 검색하였으며, 비지니스 및 바이오짐이 랫드의 에탄을 대사에 미치는 효과를 검토하여 다음과 같은 결과를 얻었다. 인체 혈중 알콜대사 촉진작용을 검색하기 위해 알콜 섭취 전과 후의 혈중 에탄올 농도를 비교하였는데, 대조군에 비해 비지니스 투여군이 30분 후부터 2시간 후까지 혈청 알콜농도가 낮게 나타났다. 대조군의 혈청 알콜농도를 100으로 하였을 때 알콜 투여 30분, 60분, 90분, 120분 경과 후 시험군은 각각 대조군의 84.3%, 89,0%, 85.9%, 75.8%를 나타내어 평균 16% 정도 낮았다. 시험군의 AUC는 대조군의 AUC의 89%로 비지니스 투여군에서 혈액내 알콜의 제거가 빠르게 진전된다는 것을 보여주었다. 또한, 랫드의 에탄을 대사에 미치는 효과를 알아보고자 바이오짐 및 비지니스 투여 후 채혈하여 혈중 에탄을 및 아세트알데히드 농도를 측정하였다. 비즈니스 투여시 혈중 알콜 농도는 알콜 투여 60분 경과후 가장 큰 감소 효과(대조군:83.70$\pm$11.80mg/이, 시험군:45.12$\pm$6.63mg/d1, 47% 감소)를 나타내었으며, 시험군의 AUC는 대조군에 비해 30% 감소하였다. 혈중 아세트알데히드 농도는 투여 60분 후 비지니스 투여군(4.56$\pm$0.51nmol/$m\ell$)이 대조군(6.45$\pm$0.64nmo1/$m\ell$)에 비해 유의성 있는 감소(29%)를 나타내었으며, 시험군의 AUC는 대조군에 비해 35% 감소하였다. 바이오짐 투여시 혈중 에탄을 농도가 알콜 투여 2시간 경과 후 가장 큰 감소 효과(대조군:49.10$\pm$5.20mg/dl, 시험군:25.90$\pm$7.16mg/d1, 47% 감소)를 나타내었으며, 시험군의 AUC는 대조군에 비해 39% 감소하였고, 혈중 아세트알데히드의 농도는 투여 60분후 시험군(3.96$\pm$0.07nmo1/$m\ell$)이 대조군(6.45$\pm$0,64nmo1/$m\ell$)에 비해 유의성 있는 감소(39%)를 나타내었으며, 시험군의 AUC는 대조군에 비해 48% 감소하였다 한편, 시험관내 에탄올 대사 효소에 대한 바이오짐의 효과를 검색해본 결과 바이오짐(2.0 $\mu\textrm{g}$/assay)에 의해 Aldehyde dehydrogenase(1.5unit/assay)의 활성이 14% 증가되었다. 본 연구의 결과로 볼 때, 비지니스 및 바이오짐은 음주 후 상승된 혈중 에탄을 농도 및 아세트알데히드의 농도를 현저히 감소시키는 효과가 있었다.

• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.25-27
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• 1988

To assess the effect of Panax ginseng on the detoxification of ethanol. we examined its effect on blood ethanol clearance in both man and experimental animals and on the rate of ethanol oxidation to carbon dioxide in experimental animals. Fourteen healthy male volunteers were subject to studies. The blood alcohol level in the test group receiving ginseng extract (3g/kg b.w.) along with alcohol (70g/65kg b.w.) was about $35\%$ lower than their control levels at 40 min after ethanol intake. When the blood alcohol level was compared on individual bases. blood alcohol concentrations in 10 subjects ranged from 32 to $51\%$ lower than their control values. The remaining 4 subjects appeared to have a high tolerance level. In experimental animals. the blood alcohol clearance was also much faster in test animals receiving ginseng along with ethanol. The rate of ethanol elimination was determined by the amount of $^{14}CO_2$ in exhaled air following the administration of [$^{14}C$] ethanol. During the first 7 1/4 hr (Phase I) after the ethanol administration. the $CO_2$ output was greater in test animals receving ginseng along with ethanol. whereas from beyond 7 1/4 hr to the near end (Phase II). the $CO_2$ output in control animals was over twice that in test animals. The present studies clearly demonstrate that ginseng promotes the overall metabolism of ethanol. resulting in an enhanced blood alcohol clearance and alcohol elimination.

• Korean Journal of Pharmacognosy
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• v.26 no.2
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• pp.148-153
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• 1995

As an initial step for evaluating hepatoprotective components against alcohol-induced toxicity, the effect of various fractions from Aloe vera on alcohol metabolism in rats were examined and the results were as follows: Water soluble fraction, after a single oral administration to rats, was found to cause a significant decrease in the serum ethanol concentration as well as enhancement of liver cytosolic ADH activity. On the other hand, the fractions soluble in organic solvent was found to cause an increase in the blood ethanol concentration and inhibit ADH activity. Further fractionation of the water soluble fraction by ultrafiltration system gave four subfractions corresponding to molecular weight and treatment of them in rats demonstrated that subfraction of M.W. > 30,000 exhibited the most potent enhancing activity of ethanol methabolism.

• The Korean Journal of Food And Nutrition
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• v.4 no.2
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• pp.207-212
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• 1991

• Journal of the Korean Society of Food Science and Nutrition
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• v.18 no.2
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• pp.229-237
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• 1989

The effects of ethanol and dietary protein levels on the calcium and phosphorus metabolism were investigated in 15-week-old male rats. Rats were divided into 4 groups ; control group(16% protein, 16 PC) and 8%(8 PE), 16%(16 PE), and 24% protein groups (24 PE) to which was given 5% ethanol mixed with their drinking water. Body weigh gain, organ weight, hemoglobin content, and hematocrit value were not affected by either ethanol or dietary protein levels. Calcium concentrations in spleen were significantly decreased in the ethanol groups than those in control group. Calcium and Phosphorus levels in femur, serum, liver, kidney, and muscle were normal. Among ethanol treated groups, fecal excretions of calcium were a little more decreased, but urinary excretions, balances and apparent absorption rate of calcium were a little more increased in higher percentage of protein group than lower percentage. Urinary phosphorus excretions in the ethanol treated groups were significantly decreased compared with the control group. Among ethanol treated groups, phosphorus balance and apparent phosphorus absorption rate of 24 PE group were significantly higher than those of 8 PE and 16 PE groups.

• Journal of Life Science
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• v.31 no.9
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• pp.796-805
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• 2021

Hepatic endoplasmic reticulum (ER) stress contributes to the development of steatosis and insulin resistance. The components of unfolded protein response (UPR) regulate lipid metabolism. Recent studies have reported an association between ER stress and aberrant cellular lipid control; moreover, research has confirmed the involvement of sterol regulatory element-binding proteins (SREBPs)-the central regulators of lipid metabolism-in the process. However, the exact role of SREBPs in controlling lipid metabolism during ER stress and its contribution to fatty liver disease remain unknown. Here, we show that SREBP-1c deficiency protects against ER stress-induced hepatic steatosis in mice by regulating UPR, inflammation, and fatty acid oxidation. SREBP-1c directly regulated inositol-requiring kinase 1α (IRE1α) expression and mediated ER stress-induced tumor necrosis factor-α activation, leading to a reduction in expression of peroxisome proliferator-activated receptor γ coactivator 1-α and subsequent impairment of fatty acid oxidation. However, the genetic ablation of SREBP-1c prevented these events, alleviating hepatic inflammation and steatosis. Although the mechanism by which SREBP-1c deficiency prevents ER stress-induced inflammatory signaling remains to be elucidated, alteration of the IRE1α signal in SREBP-1c-depleted Kupffer cells might be involved in the signaling. Overall, the results suggest that SREBP-1c plays a crucial role in the regulation of UPR and inflammation in ER stress-induced hepatic steatosis.