• Preventive Nutrition and Food Science
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• v.8 no.2
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• pp.119-123
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• 2003

To investigate the effects of the supplementation of carnitine and/or ${\gamma}$ -aminobutric acid (GABA), Sprague-Dawley male rats were orally treated with either an AIN-76 diet (control), a control diet plus ethanol (CE, 4 g ethanol/kg bw), CE plus L-carnitine (CEC, 0.5 g/kg bw), CE plus GABA (CEG, 0.5 g/kg bw), or CE plus L-carnitine plus GABA (CECG, 0.25 g/kg bw each) for 6 weeks. Serum triglyceride levels were increased in the CE group and were decreased significantly in the CEC, CEG and CECG groups. HDL-cholesterol was increased and LDL-cholesterol was decreased in the CEG and CECG groups compared with the CE group. Serum GOT and GPT levels increased by the chronic ethanol administration were decreased in the CEC group. In addition, we have evaluated the mRNA levels of carnitine palmitoyltransferase-I in those groups. Supplementation of carnitine/GABA had some recovery effects on the liver CPT-I mRNA levels which decreased by chronic ethanol administration. These results may suggest that supplementations of either L-carnitine or GABA aye effective on the recovery of chronic ethanol-related symptoms, but no combined effects were shown.

• The Korean Journal of Zoology
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• v.32 no.4
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• pp.322-328
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• 1989

The effect of dietary carnitine on ethanol-induced fattv liver and hvpertriglyceridemia was examined in an animal model. Consistent with literature, ethanol fed at 5g/Kg of b.w. to rats produced a significant increase in hepatic concentrations of total lipid, kislycerine, phospholi-pid, free cholesterol and esteriaed cholesterol as well as elevated plasma concentrations of triglvceride. It was when the ethanol diet was supplemented with D.L. camitine that there was a singini-cant reduction in the accumulation of lipids in the ethanol-compromised liver. Dietary cacti-tine was also effective in ameliorating ethanol-induced hypeuriglyceridemia. Total protein con-tents in the plasma was not varied among the groups. Ethanol의 대사과정에 관여하는 영향중에 특징적인 것으로 과유지방혈증(hyperlipidemia) 까 지방간(fatty liver)을 거쳐 간경변에 이르는 간에 관계하는 일련의 증상들을 들 수 있다. 본 실험에서는 만성적 ethanol의 지방대사 장해에 대한 D.L.-carnitine의 효과에 대해 고찰하였다. 실험용 횐쥐를 사용하여 실험군(ethanol group)에게 체중 kg당 5g의 ethanol(30% in saline)을 투여하여 알콜유발성 지방간과 과유지방혈증을 일으키고, 그 실험군 흰쥐들에게 carnitine(0.4 mg/g of body weight)을 첨가하여 그 효과를 관찰하였다. 그 결과 carnitine을 첨가하여 투여한 흰쥐들에서 ethanol처리군과 비교하여 볼 때 간과 혈장에서 지방축적이 현저히 감소하는 것을 관찰할 수 있었다.

• The Korean Journal of Zoology
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• v.32 no.4
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• pp.351-357
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• 1989

To investigate the effect of alcohol on the ultrastructural changes of liver the experiment was undertaken by dividing in 3 groups (control, alcohol and alcohol-camitine groups). Chronic administration of ethanol to adult rats led to striking fat accumulation and ultrastructural changes in the liver. Mitochondrial abnormalities. dilation of endoplasmic reticulum, focal cytoplasmic degradation, dilation of bile canalicli and swelling of nucleus were observed. In alcohol-carnitine group, there were less fat accumulation and ultrastructural changes than alcohol group. These alterations suggest that ethanol is very toxic to the liver and carnitine prevents fat accumulation induced by alcohol. 알콜이 흰쥐 간장의 미세구조에 미치는 영향을 관찰하기위해 대조군, 알콜 처리군, 알콜-carnitine처리군으로 나누어 실험하였다. 만성적인 알콜 투여는 간에서의 지방축적을 유발하였으며 미토콘드리아의 이상, 소포체의 팽대, 세포질의 손상 Bile canaliculi의 확장 및 핵의 수축 등의 미세구조적 변화를 가져왔다. 알롤- carnitine으로 처리한 군에서는 지방의 축적과 미세구조의 변화가 알콜 처리군에서 보다는 약하였다. 이러한 구조적 변화는 알콜이 간에 매우유독하며 carnitine은 알콜에 의해 유발된 지방의 축적을 방지해 보여주는 것으로 사료된다.

• Preventive Nutrition and Food Science
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• v.4 no.1
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• pp.75-78
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• 1999

Acetylcarnitine, a metabilite of carnitine, has been porven to be a potent inhibitor of ethanol oxidation in hepatocytes. It inhibits the activity of alcohol dehydrognase (ADH), but not the microsomal ethanol oxidizing system. which was significatly inhibited by acetylcarnitine at NAD ; acetylcarnitine $\leq$1. the main objectives of his study were to ascertain the interaction between acetylcarnitine and NAD on ADH activity and to elucidate whether different species have different effects. Tehpost-mocrosomal supernatant (PMS) was prepared from normal rat, guinea pig, mouse and broilers by differential centrifugation . Horse and yeast ADH were purchased from the Sigma Chemical Co. Prepared and purchased ADH are used for determination of ADH activity in the presence or absence of carnitine and acetylcar- nitine. Binding studies showed that acetylcarnitine did bind to ADH in a dose realted manner when low NAD ; acetylcar- nitine ratio was provided. It was found that the inhibitionof ADH activity occurred only when NAD concentration was less than the inhibitor concentration . Crystalline and crude ADH preparation from different vertebrate species wer inhibited by acetylcarnitine, whereas the yeast ADH was not affected by acetylcarnitine.

• Preventive Nutrition and Food Science
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• v.15 no.3
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• pp.196-205
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• 2010

This study evaluated the effects of carnitine and/or GABA supplementation on immune function, lipid profiles and some vitamins in mice chronically administered alcohol. BALB/c mice were fed with either AIN-76 diet (N), control diet plus alcohol (4 g/kg bw, E), E plus 0.5 g/kg bw carnitine (EC), E plus 0.5 g/kg bw GABA (EG), or E plus 0.5 g/kg bw carnitine plus 0.5 g/kg bw GABA (ECG) for 6 weeks. Administrations of the carnitine and/or GABA prevented alcohol-induced increases in triglyceride concentrations in serum and liver. However, there was no difference among the supplemented groups. Serum vitamin E concentration was higher in mice supplemented with EC and EG, but not in mice given ECG. Phagocytic activity of peritoneal macrophages was increased in EG group compared with E group. The subpopulations of murine splenocyte's TH cells were increased significantly in EC and ECG groups. These data suggest that immune function, lipid profiles and some immune-related lipid soluble vitamins were positively changed by supplementation of carnitine or GABA, but do not show any synergistic effect of mixed supplementation.

• Korean Journal of Human Ecology
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• v.9 no.1
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• pp.71-80
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• 2006

To investigate the effects of the supplementation of Stevia. Rebaudian Bertoni on serum and hepatic lipid levels and enzyme activities in rat administered with ethanol chronically. Sprague-Dawley male rats were orally treated with either an AIN-76 diet(C, control), a control diet plus ethanol(E, 4g/kg bw), E plus stevia extract-1(ES1, 1ml/kg bw), or E plus stevia extract-2(ES2, 2ml/kg bw) for 7 weeks. Serum triglyceride levels were increased in the E group and were decreased in the ES 1 group. Liver triglyceride levels were decreased significantly in the ES2 groups and Total-cholesterol were decreased in the ES1, ES2 groups compared with the E group. Liver $\gamma-GTP$ levels were decreased significantly in the ES1, ES2 groups compared with the E group. In addition, we have evaluated the serum or liver carnitine levels in those groups. Liver TCNE levels were increased significantly in the ES1, ES2 compared with the E group. These results may suggest that supplementation of Stevia. Rebaudian Bertoni has effects on the recovery of chronic ethanol-related diseases.

• Journal of Ginseng Research
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• v.23 no.2 s.54
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• pp.115-121
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• 1999

Effects of single and repeated administration of various nootropic candidates were examined on impaired acquisition by single oral administration of 3 g/kg ethanol (EtOH) in step through test. The inhibitory effect of EtOH on acquisition was significantly reduced by single picrotoxin, but not affected by diazepam, acetyl-L-carnitine and apomorphine. Single or repeated red ginseng total saponin and deprenyl, single piracetam, repeated N-methyl-D-glucamine, but not single or repeated protopanaxadiol, protopanaxatriol and centrophenoxine significantly ameliorated the impairment of acquisition by EtOH. On the other hand, the inhibitory effect of repeated red ginseng total saponin but not that of repeated N-methyl-D-Glucamine, was significantly blocked by pretreatment of $\alpha$-methyl-$\rho$-tyrosine, a inhibitor of catecholamine synthesis. Whereas, the inhibitory effect of repeated deprenyl on EtOH amnesia was exaggerated by $\alpha$-methyl-$\rho$-tyrosine. These results suggest that the amelioration processes of drugs on ethanol amnesia involve complex mechanism between the central GABAergic and dopaminergic neuronal activity in memory and learning, although the effects of repeated drugs administration are not yet clear.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.1
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• pp.168-174
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• 1998

This study was conducted to determine whether Mildronate, an analogue of carnitine, influences blood alcohol concentration and hang-over syndrome in rabbits and healthy college male students. In the animal study, ten rabbits were randomly divided into two groups. One hundred mg per 1kg body weight of Mildronate was injected twice into five rabbits before injecting 50% ethanol; the rest of rabbits were injected with saline. The human study was performed with two sections. Each section of the study was conducted by a two-phase cross-over design with a four day wash-out period. All volunteers took Mildronate in one phase, and took a placebo in the next phase. The difference between the two sections was related to the time of taking the Mildronate pill and the amount of alcohol consumed. Blood alcohol concentrations were not significantly different between in those taking Mildronate and in those taking the placebo in both the human and the animal study. However, the concentration of serum aspartate aminotransferase(AST, GOT), the indicator of liver cell damage, was lowered in those taking Mildronate, compared to those taking the placebo. Also, headache and heartburn among hang-over syndrome patients were less severe with Mildronate. In conclusion, taking Mildronate prior to drinking alcohol can somewhat reduce liver cell damage and hang-over syndrome without stimulating alcohol metabolism.

• Journal of Physiology & Pathology in Korean Medicine
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• v.31 no.3
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• pp.159-166
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• 2017

Through this study, the authors investigated the anti-steatosis effects of the Amomum cardamomum ethyl acetate fraction in free fatty acids (FFAs)-induced human hepatocellular carcinoma HepG2 cells. The ethyl acetate fraction of Amomum cardamomum (ACEA) was extracted with 70% ethanol and then the extract was evaporated using a rotary evaporator prior to sequential fractionation. Human hepatocellular carcinoma were treated with different concentrations of ACEA in the presence and absence of FFAs. To demonstrate the reactive oxygen species (ROS) scavenging activity, DCFDA level was analyzed by using in vitro assay system. Cell viability, lipid accumulation, intracellular triglycerides, malondialdehyde (MDA), liver steatosis related signaling molecules and inflammatory cytokines such as interleukin (IL)-6, 8, tumor necrosis factor-alpha ($TNF-{\alpha}$) were also investigated. As results, ACEA inhibited the FFAs-induced ROS, lipid accumulation, intracellular triglycerides, and MDA in a dose dependent manner. Treatment of human hepatocellular cells with ACEA induced the phosphorylation of 5' adenosine monophosphate-activated protein kinase (AMPK) and carnitine palmitoyltransferase I (CPT1) expression using western blot analysis. ACEA also potently suppressed the FFAs-induced inflammatory cytokines including IL-6, IL-8 and $TNF-{\alpha}$. These results suggest that the ethyl acetate fraction of Amomum cardamoum extract own inhibitory effects of liver steatosis by inhibiting ROS, lipid accumulation, intracellular triglycerides, MDA through AMPK signaling and anti-inflammatory actions.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.4
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• pp.401-408
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• 2017

Salvia plebeia R. Br. (Lamiaceae) has been used in folk medicines in Asian countries, including Korea and China, to treat inflammatory diseases. The focus of our research was on the anti-adipogenic activity of ethanol extract from Salvia plebeia R. Br. (SPE) in 3T3-L1 adipocytes. This study investigated inhibition of differentiation and lipogenesis upon SPE treatment in 3T3-L1 cells. The results reveal that SPE at non-cytotoxic concentration significantly suppressed triglyceride accumulation and reduced expression of peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding protein-alpha, and sterol regulatory element-binding protein as adipogenic transcription factors in 3T3-L1 adipocytes compared to non-treated control cells. Inducible phosphorylation of AMP-activated protein kinase, acetyl CoA carboxylase, and hormone-sensitive lipase as well as carnitine palmitoyltransferase-1 mRNA expression increased upon SPE treatment, which suppressed expression of fatty acid synthase. In conclusion, these results demonstrate that SPE can inhibit expression of adipogenic genes in 3T3-L1 adipocytes. Our study suggests that SPE has potential anti-obesity effects and is a novel therapeutic functional agent with anti-adipogenic activity via reduction of lipogenesis.