본 연구는 폐경 후 비만 여성의 동물모델을 이용하여 수영운동이 비알코올성 지방간에서 염증에 미치는 영향을 조사하였다. 실험동물은 수영운동을 하지 않은 모의수술군(S/N), 수영운동을 하지 않은 난소절제 수술군(O/N) 및 수영운동을 실시한 난소절제 수술군(O/S)으로 구분되어 8주 동안 고지방식이 사료를 섭취하면서 사육되었다. 간 조직의 지방축적, 간 무게 및 혈청 속 AST와 ALT는 S/N에 비해 O/N 에서 증가하였으나, O/N에 비해 O/S에서는 감소하였다. S/N에 비해 O/N는 간 조직에서의 IκBα의 유전자 발현이 감소하였고 MCP-1, IL-6 및 TNF-α의 유전자 발현은 증가하였다. 그러나 O/N에 비해 O/S는 간 조직에서의 IκBα이 증가하였고 MCP-1, IL-6 및 TNF-α의 유전자 발현은 감소하였다. 결론적으로 본 연구는 난소절제 후 고지방식이의 섭취로 비만이 유도된 비만 쥐에서 수영운동이 비만으로 유도 된 비알코올성 지방간에서 염증을 개선함으로써 건강증진에 효과적임을 제시하였다.

본 연구는 스트렙토조토신에 의해 유도한 당뇨병, 알코올성 간 손상 실험용 랫드에서 혈액 지질 감소, 당뇨병 및 알코올성 간 손상 예방에 미치는 지장김치 추출물의 경구투여 효과를 조사하였다. 당뇨병 모델동물에서, 혈액 지질 프로파일, ALT, AST 수준은 DC (당뇨병 대조군)와 비교할 때 김치추출물 투여군에서 낮아졌으며 혈당은 DCJK (DC+지장김치 추출물 경구투여군)가 DCCK (DC+일반김치 추출물 경구투여군)에 비해 낮았다. 인슐린 수준은 NC (정상대조군), DCJK > DCCK > DC 순서로 높게 나타났다. 알코올성 간 손상 모델동물에서, 혈액 ALT, AST, 빌리루빈 농도는 AC (알코올 대조군, 일일 소주 1병 섭취군) > ACCK (AC+일반김치 추출물 경구투여군) > ACJK (AC+지장김치 추출물 경 구투여군) > NC 순서로 낮았다. 간 조직의 임상병리학적 소견은 AC에서 가장 심각한 손상을 보였으나 소주1병과 김치 추출물 특히, 지장김치 추출물 경구투여군은 일반김치 추출물 경구투여군에 비해서 회복되는 속도가 개선되었다. 결과는 당뇨병 및 알코올성 간 손상 모델동물에서 지장김치의 섭취가 혈액 지질 프로파일, 혈당, ALT, AST 수준을 낮추고 인슐린 분비능력을 개선하여 줌으로써 항당뇨 및 알코올성 간 손상 보호효과를 갖는다는 사실을 보여준다.

본 연구의 목적은 oleic acid로 지방생성이 유도된 HepG2 세포에서 자색옥수수 색소 1호 포엽 및 속대 추출물이 간 세포 내 지방생성에 미치는 영향을 구명하는 것이다. 자색옥수수 색소 1호 포엽 및 속대 추출물에 의한 HepG2 세포 내 지방 축적의 변화를 확인하기 위하여 배양된 세포에 oleic acid로 지방 축적을 유도하고 추출물에 의한 중성지방생성 억제 효과를 측정하였으며 추출물을 처리하지 않은 대조군과 추출물을 처리한 실험군의 지방합성 및 축적에 관련된 유전자와 단백질 발현량을 RT-PCR과 Western blot을 통하여 측정하였다. Oil Red O와 Nile Red 염색을 통하여 추출물의 처리로 HepG2 세포 내 중성지방 축적이 억제된 것을 확인하였다. RT-PCR에 의하여 mRNA 발현량을 측정한 결과, oleic acid에 의하여 지방 생성이 유도된 대조군에 비하여 모든 추출물 처리군의 SREBP-1c와 SREBP-1a 유전자 발현량이 유의적으로 감소되었다. Western blot을 실시하여 p-AMPK, p-SREBP1, PPARα, FAS 단백질의 발현량을 측정한 결과, 간에서 지질대사에 관여하는 주요 인자인 SREBP1 단백질의 발현은 추출물의 처리 농도에 따라 유의하게 감소하였으며 지방산의 생합성 경로에 관여하는 주요 효소인 FAS의 단백질 발현향은 모든 처리 농도에서 현저하게 감소된 것이 확인되었다. 본 연구 결과는 자색옥수수 색소 1호 포엽 및 속대 추출물이 간세포 내에서 중성지방의 축적을 억제시키고 지질 합성에 관련된 유전자 및 단백질의 발현을 억제시킴으로써 간 세포 내 지질 축적을 완화할 수 있는 기능성 소재로의 활용가치가 높다고 판단된다.

This study was performed to investigate the effects of Acer tegmentosum Maxim. extract (ATE) on non-alcoholic fatty liver in Sprague Dawley (SD) rats. During oral administration of ATE, non-alcoholic fatty liver was induced by treatment with DL-ethionine. The lipid, total cholesterol (T-CHO) and malondialdehyde (MDA) in the liver tissue of ATE-fed rats showed lower levels, as compared to ATE-unfed rats. In ATE-fed rats, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl transferase (GGT) were lower than the case of ATE-unfed rats. Oil red staining of the liver showed that the lipid deposits were decreased by feeding ATE. These results strongly indicated that ATE has positive effects of protection against non-alcoholic fatty liver formation.

The role of cytochrome P-450 2E1 (P450 2E1) in the early phase of alcoholic fatty liver was examined. Female rats were pretreated with either allyl sulfide (200 mg/kg, po), disulfiram (500 mg/kg, po), YH 439 (250 mg/kg, po) or pyrazine (200 mg/kg/day × 2 days, ip). Marked changes in carbon tetrachloride-induced hepatotoxicity and carboxyhemoglobin (COHb) elevation due to dichloromethane administration were observed in rats treated with one of the P450 2E1 modulators. A single dose of ethanol (6 g/kg, po) increased the hepatic triglyceride contents approximately 2 fold, which was inhibited completely by YH 439 pretreatment. However, the other P450 2E1 modulators failed to alter the ethanol-induced hepatic triglyceride accumulation. In vitro hepatic microsomal enzyme activity was determined in 4 week old premature and 12 week old adult rats. Aminopyrine-N demethylation was not different, but p-nitrophenol hydroxylation and p-nitroanisole O-demethylation were significantly higher in premature rats compared to adult indicating that the P450 2E 1 activity decreases with the maturity of rats. However, no difference in the triglyceride accumulation induced by an intraperitoneal dose of ethanol (3 g/kg) was noted between premature and adult rats. The results suggest that the P450 2E1 activity dose not play an important role in the induction of acute alcoholic fatty liver.

Alcoholic fatty liver disorder has become a frequent health concern worldwide. To investigate the effects of Brassica oleracea (B. oleracea) sprout extract (BOE), the present study was designed with alcoholic fatty liver in the rat. Initially, the effects of BOE on liver parameters were examined. Male rats were divided into five groups. The normal control group was fed the normal diet, and the BOE group was fed the high fat diet and ethanol with/without BOE for 4 weeks. After 4 weeks feeding period, rats were sacrificed and their livers and blood were used for fatty liver-related biomarkers analyses. As a result, BOE ameliorated fatty liver-related enzymes profiles in liver tissues and also reduced blood alcohol concentration in rat model. We demonstrated that BOE protected the high fat diet and alcohol-induced fatty liver in rat model. Furthermore, BOE increased detoxificative abilities against alcohol.

Background : Non-alcoholic fatty liver disease (NAFLD) is caused by obesity, type 2 diabetes mellitus, dyslipidemia, and genetic factors. Also, hyperinsulinemia directly promotes fat accumulation in hepatocytes. Therefore, it is very important to suppress the most common risks of NAFLD, such as obesity and insulin resistance. In this context, we evaluated for the effects of black ginseng (BG) extract on lipid accumulation inhibition and degradation in hepatocytes. Methods and Results : The aim of this study is to figure out the potential anti-lipogenic effects and the underlying mechanism of BG extract in a cellular-, type 2 diabetes mellitus (T2DM) animal model associated with NAFLD. T2DM animal used C57BL/KsJ db/db mouse (M. 6 wk, n = 56), treated with extract of BG and Red ginseng (RG) (each 100 and 900 ㎎/ ㎏/day, p.o) for 6 weeks. BG markedly reduced palmitate-induced intracellular lipid accumulation in HepG2 cells. On histology of liver tissues of T2DM animal, macrovesicular lipid droplets in cytoplasm of hepatocytes were decreased both RG and BG-treated groups. In liver tissue, BG-treated groups suppressed CCAAT/enhancer binding protein-α (C/EBP-α), sterol regulatory element-binding protein-1c (SREBP-1c) expression, and SREBP-1c mediated induction of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) proteins related to the induction of adipose differentiation. Futhermore, adenosine monophosphate (AMP)-activated protein kinase (AMPK) activity was significantly increased in BG-treated groups compared to RG-treated groups. It is also found that peroxisome proliferator-activated receptor-α (PPAR-α) highly expressed in BG-treated groups. Conclusion : Our results suggest that black ginseng extract has an anti-adipogenic and anti-lipogenic effects in the liver when administered as a food supplement and has potential as a therapeutic agent for obesity and T2DM induced NAFLD.

This study was undertaken to evaluate the association between the appearance of hypodense hepatic nodules on dynamic CT images and acute alcoholic hepatitis in patients with alcoholic cirrhosis. Sixty-two patients (male:female=57:5, mean age=51.4±10.9 years) with alcoholic cirrhosis were included. Patients were divided into 3 groups; group A (nodules, n=23), group B (fatty liver < 40 Hounsfield unit (HU) without nodules, n=18), and group C (control, n=21). Liver nodules in Group A had characteristic low density during pre- and all post-contrast phases versus liver parenchyma and fewer or complete resolution of nodules on follow up CT after alcohol withdrawal. Densities (HU) of nodules and hepatic parenchyma, ascites scores, and laboratory values were analyzed. Mean densities of hepatic parenchyma in groups A and B were significantly lower than in the control group. Serum bilirubin, AST (aspartate transaminase), ALT (alanine transaminase), PT (prothrombin time), and ascites scores were significantly higher in group A than in the other two groups. As numbers of liver nodules increased nodules’ attenuation decreased. Mean serum AST and ALT were higher in patients with many nodules than in patients with few nodules. Hypodense hepatic nodules in alcoholic steatohepatitis in patients with alcoholic cirrhosis are probably benign nodules resulting from focal steatosis or hepatocellular necrosis rather than metastases.