• Journal of Korean Medicine for Obesity Research
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• v.22 no.2
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• pp.158-166
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• 2022

Objectives: The purpose of this meta-analysis was to evaluate the effects of berberine on non-alcoholic fatty liver disease (NAFLD) through a systematic review and meta-analysis. Methods: We searched seven electronic databases for studies through October 2022. All randomized controlled trials (RTCs) of berberine were included. Data extraction and risk of bias assessments were performed by two independent reviewers. The RevMan 5.4.1 program was used for meta-analysis. Results: A total of 279 relevant studies were identified, and 6 eligible RCTs were included to study the efficacy berberine on NAFLD. The six selected trials are studies on the effect between berberine and conventional treatment combined treatment versus conventional treatment. Liver function tests, blood lipid levels, and blood glucose levels were assessed. Combination treatment with berberine, ursodeoxycholate acid, metformin, and monascus purpureus showed statistically significant improvements in liver function levels, blood lipid levels, and blood glucose levels compared to conventional treatment alone. However, there was no significant efficacy of berberine combination dietary, exercise than control group on NAFLD. The meta-analysis results of examining 4 RCTs comparing the therapeutic efficacy of berberine showed statistically significant improvement in the liver function test, blood lipids levels, blood glucose levels. Conclusions: This study suggests that berberine has positive efficacy on blood lipids, blood glucose liver function, fatty liver condition of NAFLD. However, the level of evidence is low because of small effect size,so further investigation is needed.

• Biomedical Science Letters
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• v.14 no.4
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• pp.225-231
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• 2008

Non-alcoholic fatty liver disease (NAFLD) is associated with various metabolic abnormalities, including central obesity, type 2 diabetes, dyslipidemia, and high blood pressure. This suggests that NAFLD may represent the hepatic manifestation of the metabolic syndrome. In this study, we investigated unfavorable effects NAFLD on components of metabolic syndrome in post-menopause women. Eight hundred sixty-nine postmenopausal women were recruited for this study. The diagnosis of fatty liver was based on the results of abdominal ultrasonography. Serum levels of fasting glucose, total cholesterol, triglyceride, and HDL-cholesterol were measured. The prevalence of component of metabolic syndrome such as hypertension, hyperglycemia, hypertriglyceridemia, and low-HDL-cholesterol was significantly higher in subjects with NAFLD as compared with those without NAFLD. The moderate to severe grade of NAFLD presented higher levels of serum fasting glucose, fasting insulin, HOMA-IR, total cholesterol, and triglycerides than the mild NAFLD and the normal group. In conclusion, metabolic syndrome risk was increased in post-menopause women with NAFLD as compared with those without NAFLD. The severity of NAFLD affected metabolic syndrome risk factors. The optimal strategy for the treatment of NAFLD is likely to include lifestyle modifications and therapy to improve insulin resistance.

• Journal of Food Hygiene and Safety
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• v.11 no.4
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• pp.291-297
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• 1996

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$\times$2 days, ip). Marked changes in carbon tetrachloride-induced hepatotoxicity and caboxyhemoglobin (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. 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.

• Journal of Preventive Medicine and Public Health
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• v.41 no.1
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• pp.39-44
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• 2008

Objectives : This study was conducted to investigate the associations of non alcoholic fatty liver with metabolic syndrome and the serum carotenoids. Methods : This study was conducted in a general hospital in South Korea from November, 2004 to August, 2005. The study subjects were 350 sampled persons who were aged from 40 years and older (males : 180, females : 170). They were grouped into the normal, mild and severe groups according to fat accumulation in their livers, as determined by ultrasonography. We analyzed the association between non alcoholic fatty liver and metabolic syndrome by multiple logistic regression analysis and we analyzed the association between non alcoholic fatty liver and the serum carotenoids by a general linear model(ANCOVA). Results : After adjustment for the effect of potential covariates, the prevalence of metabolic syndrome was associated with fat accumulation in the liver (p trend <0.001). If the odds ratio of normal group is 1.00, then that of the mild group is 2.80 (95% C.I=1.17-6.71) and that of the severe group is 7.29 (95% C.I=2.76-19.30). The prevalence of metabolic alterations fitting the criteria of metabolic syndrome, according to the class of fat accumulation in the liver, was significantly increased, except for criteria of high blood pressure, a large waist circumference and low HDL (high density lipoprotein) cholesterol level (p trend <0.001). The level of serum ${\beta}$-carotene was decreased according to the class of fat accumulation in the liver (p trend=0.036), but the levels of serum ${\alpha}$-carotene, lycopene, ${\beta}$-cryptoxanthin and lutein were not decreased. Conclusions : This study shows that non alcoholic fatty liver was associated with metabolic syndrome and with the serum ${\beta}$-carotene level.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.22 no.5
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• pp.470-478
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• 2019

Purpose: The incidence of non-alcoholic fatty liver disease (NAFLD) in children is gradually increasing. The aim of this study was to investigate the use of serum adiponectin and soluble adiponectin receptor 2 (soluble Adipo R2) levels for the diagnosis of fatty liver disease in obese and overweight children. Methods: The study included 51 obese and overweight children between the ages of 6 and 18 years diagnosed with NAFLD using ultrasonography and 20 children without fatty liver disease. Patients whose alanine transaminase level was two times higher than normal (${\geq}80U/L$) were included in the non-alcoholic steatohepatitis (NASH) group. Results: NASH was observed in 11 (21.6%) of the patients with NAFLD. The incidence of obesity was higher in patients with NASH (80% and 45%, p=0.021). While the adiponectin levels were similar in patients with NAFLD and those without, they were below the normal level in the whole study group. Adiponectin and soluble Adipo R2 levels of patients with NASH were lower than those in patients without NASH; however, this difference was not statistically significant (p=0.064 and p=0.463). Soluble Adipo R2 levels in obese patients with NAFLD were higher than those in obese children without NAFLD (p<0.001). Conclusion: Soluble adiponectin receptor 2 level is a noninvasive marker that can be used for the diagnosis of NAFLD in obese children.

• Archives of Pharmacal Research
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• v.29 no.9
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• pp.768-776
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• 2006

Non-alcoholic fatty liver disease (NAFLD) is common in obesity. However, weight reduction alone does not prevent the progression of NAFLD to end-stage disease associated with the development of cirrhosis and liver disease. In a previous experiment, 50% ethanol extract of Acanthopanax senticosus stem bark (ASSB) was found to reduce body weight and insulin resistance in high fat diet-induced hyperglycemic and hyperlipidemic ICR mice. To evaluate the anti-steatosis action of ASSB, insulin-resistant ob/ob mice with fatty livers were treated with ASSB ethanol extract for an 8 week-period. ASSB ethanol extract reversed the hepatomegaly, as evident in reduction of % liver weight/body weight ratio. ASSB ethanol extract also specifically lowered circulating glucose and lipids, and enhanced insulin action in the liver. These changes culminated in inhibition of triglyceride synthesis in non-adipose tissues including liver and skeletal muscle. Gene expression studies confirmed reductions in glucose 6-phosphatase and lipogenic enzymes in the liver. These results demonstrate that ASSB ethanol extract is an effective treatment for insulin resistance and hepatic steatosis in ob/ob mice by decreasing hepatic lipid synthesis.

• Toxicological Research
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• v.24 no.2
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• pp.113-117
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• 2008

Chronic exposure to ethanol induces cumulative damage to the liver starting from fatty infiltration to cirrhosis depending on the dose and duration of exposure. The whole process leading to the development of alcoholic liver disease is very complex and the mechanisms involved are not fully understood. Among many experimental animal models, Lieber-DeCarli liquid diet provides moderate to severe pathophysiological outcome depending on the compositional changes. In the present study, we investigated the temporal changes in the early phase hepatic disease in rats fed with standard Lieber-DeCarli diet. Male Wistar rats were fed with Lieber-Decarli ethanol diet for 6 weeks and the liver samples were obtained after 2, 4 and 6 weeks. Mild fatty infiltration was observed in 2 weeks of feeding and it became evident in 4 and 6 week samples. The level of hepatic triglyceride showed a good agreement with the data obtained in the pathological analysis. Feeding mice with ethanol diet resulted in the maturation and translocation of SREBP-1 to nucleus in the liver. Western blot analysis of the pooled liver sample of control and ethanol fed animals showed a clear-cut time-dependent increase in the expression of nSREBP-1. These data provide important information for selecting proper time point in experimental intervention study in the field of drug development for alcoholic liver disease.

• Herbal Formula Science
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• v.28 no.2
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• pp.179-187
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• 2020

Objectives : This study investigated the hepatoprotective effects effects of Jageum-jung extract on alcohol-induced liver disease mice model. Methods : Alcoholic liver disease was induced by Ethanol in C57/BL6 male mice, which were fed Lieber-DeCarli liquid diet containing ethanol. Jageum-jung (100,200 and 300 mg/kg bw/day) were orally administered daily in the alcoholic fatty liver disease mice for 16 days. Results : The results indicate that Jageum-jung promotes hepatoprotective effects by significantly reducing aspartate transaminase (AST) and alanine transaminase (ALT) levels as indicators of liver damage in the serum. Furthermore, Jageum-jung decreased accumulation of triglyceride and total cholesterol, increased levels of superoxide dismutase (SOD) and glutathione (GSH) in the serum of the alcoholic fatty liver disease mice model. Additionally, it improved the serum alcohol dehydrogenase (ADH) activity. Conclusions : This study confirmed the anti-oxidative and hangover elimination effects of Jageum-jung extract, and suggests the possibility of using Jageum-jung to treat alcholic liver disease.

• The Journal of the Korea Contents Association
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• v.9 no.6
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• pp.237-246
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• 2009

This study was carried out to investigate of the associations of Alcoholic & Nonalcoholic fatty liver disease(AFLD & NAFLD) with metabolic syndrome(MS) defined by IDF criteria. We conducted a cross-sectional study of 799 adult males with alcohol consumption underwent laboratory investigation(control 297, alcoholic 206, nonalcoholic 296). The ultrasound scan of the liver was performed to determine the presence and the severity of FLD. We analyzed the association between the severity of AFLD & NAFLD and MS by logistic regression analysis. The distribution of metabolic syndrome was 7.4%, 48.8%, 34.9% in control, AFLD & NAFLD. The association of blood pressure, glucose, triglycerides, obesity were risk factor in AFLD & NAFLD. According to the severity of FLD, AFLD was significantly increased with MS, Obesity, low HDL-cholesterol. MS, High triglycerides was increased significantly in NAFLD(p<0.05). The prevalence of AFLD & NAFLD was increased with increasing the number of features of metabolic syndrome. This study shows that AFLD & NAFLD was closely associated with MS and its components. The patients of AFLD & NAFLD should managed and monitored to prevent metabolic abnormalities.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.11 no.6
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• pp.2093-2098
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• 2010

Insulin resistance plays a central role in fatty liver, a part of the metabolic syndrome. This study examined the relationship between fatty liver, metabolic abnormalities and mitochondrial DNA [mtDNA] copy number in peripheral blood that is correlated with diabetes or metabolic markers. Fatty liver was assessed by questionnaire on alcohol consumption and abdominal ultrasonography. MtDNA copy number in peripheral leukocytes was measured by a real-time quantitative polymerase chain reaction [PCR]. Among 445 subjects, 148 subjects had hepatic steatosis and 297 were controls. mtDNA copy number was significantly lower in fatty liver group in comparison with that of normal finding group. This result is similar in both groups, alcoholic or non-alcoholic fatty liver group. MtDNA copy number was inversely correlated with alanine aminotransferase [ALT], aspartate aminotransferase [AST], gamma-glutamyltransferase [$\gamma$-GTP], body mass index [BMI], waist circumference, diastolic blood pressure, and free fatty acid. MtDNA copy number in peripheral leukocytes was associated with fatty liver and insulin resistance related factors.