• Journal of Life Science
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• v.19 no.2
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• pp.185-191
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• 2009

Although alcohol drinking may cause fatty liver to induce hepatocytic injury, other factors lead to it. We designed this study to investigate the differences in serum iron, cardiac, and biochemical indices in men with fatty liver and the difference between alcohol drinkers (Alcohol group) and non-drinkers (Non-alcohol group). The alcohol group had higher body indices than the non-alcohol group. Systolic and diastolic blood pressure (SBP and DBP), and right and left intraocular pressure in the alcohol group were higher than those in the non-alcohol group. Hemoglobin, hematocrit, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and monocyte counts were higher in the alcohol group than in the non-alcohol group. Alanine aminotransferase, ${\gamma}$-glutamyltranspeptidase, total cholesterol, triglyceride, low-density lipoprotein cholesterol, glucose, creatinine, uric acid, iron, total iron binding capacity, and ferritin levels in the alcohol group were greater than those in the non-alcohol group. The present data reveals that alcohol-induced fatty liver has more elevated level of iron indices than in non-alcohol fatty liver as well as biochemical and cardiac indices, indicating that alcohol- induced fatty liver may cause possibility of adult diseases including cardiovascular disease and metabolic syndrome.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.12 no.7
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• pp.3130-3137
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• 2011

The present study was to elucidate such a relationship by comparing the coronary risk factors with and without fatty liver adjusted for age and/or BMI. Study subjects were 665 women of 30 years and over, who underwent health package check-up at the health promotion center of an university hospital from July, 2009 to June, 2010. As a results, the prevalence rates of fatty liver of study subjects were 11.6%, and the rates were significantly higher in older age group, in the group of higher level of BMI. The group of subjects with fatty liver had significantly lower mean HDL-cholesterol and higher levels of body fat rate, TG, TC, LDL-cholesterol, FBS and ALT, then those parameters in subjects without fatty liver, even after adjustment for age and/or BMI. In age and BMI adjusted logistic regressions, The odds ratio of fatty liver was increased significantly as there is an increase in the abnormal group with TG, TC, LDL-C and ALT.

• Journal of the Korean Society of Radiology
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• v.12 no.5
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• pp.623-630
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• 2018

Non-alcoholic fatty liver disease is the most common cause of chronic liver diseases. This study was to characterize early hepatic lipid changes in fatty liver rat model by in vivo short-echo time(TE) $^1H$-MRS(Proton - Magnetic Resonance Spectroscopy). Each the examinations were measured from liver parenchyma in rats at 0, 2, 4, 6, 8 weeks followed by high fat diet, respectively. Significant increase in lipid signals. 0.9, 1.3, 2.3, 2.8, and 5.3 ppm was found in animals with 2 weeks(p<0.01). Therefore, $^1H$-MRS is useful in detecting and characterizing various hepatic lipid alterations as early as 2 weeks for the start high fat diet.

• Preventive Nutrition and Food Science
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• v.21 no.3
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• pp.171-180
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• 2016

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases associated with an altered lifestyle, besides genetic factors. The control and management of NAFLD mostly depend on lifestyle modifications, due to the lack of a specific therapeutic approach. In this context, we assessed the effect of carrot juice on the development of high fructose-induced hepatic steatosis. For this purpose, male weanling Wistar rats were divided into 4 groups, fed either a control (Con) or high fructose (HFr) diet of AIN93G composition, with or without carrot juice (CJ) for 8 weeks. At the end of the experimental period, plasma biochemical markers, such as triglycerides, alanine aminotransferase, and ${\beta}$-hydroxy butyrate levels were comparable among the 4 groups. Although, the liver injury marker, aspartate aminotransferase, levels in plasma showed a reduction, hepatic triglycerides levels were not significantly reduced by carrot juice ingestion in the HFr diet-fed rats (HFr-CJ). On the other hand, the key triglyceride synthesis pathway enzyme, hepatic stearoyl-CoA desaturase 1 (SCD1), expression at mRNA level was augmented by carrot juice ingestion, while their protein levels showed a significant reduction, which corroborated with decreased monounsaturated fatty acids (MUFA), particularly palmitoleic (C16:1) and oleic (C18:1) acids. Notably, it also improved the long chain n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA; C22:6) content of the liver in HFr-CJ. In conclusion, carrot juice ingestion decreased the SCD1-mediated production of MUFA and improved DHA levels in liver, under high fructose diet-fed conditions. However, these changes did not significantly lower the hepatic triglyceride levels.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.24 no.1
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• pp.54-64
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• 2021

Purpose: Nonalcoholic fatty liver disease (NAFLD) is the most frequent cause of chronic liver diseases in both adults and children with obesity. The aim of this study was to compare the changes in liver enzymes and metabolic profile in adolescents with fatty liver following selected school-based exercise (SBE) and high-intensity interval training (HIIT) interventions. Methods: In a semi-experimental study, 34 obese male adolescents with clinically defined NAFLD were divided into the HIIT (n=11, age=12.81±1.02 years, body mass index [BMI]=26.68±2.32 kg/㎡), selected SBE (n=11, age=13.39±0.95 years, BMI=26.47±1.74 kg/㎡), and control (n=12, age=13.14±1.49 years, BMI=26.45±2.21 kg/㎡) groups. The ultrasonography NAFLD grade, peak oxygen uptake (VO2peak), lipid profile, insulin resistance, and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels of the participants were measured before and after the exercise interventions. Results: The BMI, waist-to-hip ratio, and body fat percentage of the participants decreased, and a significant increase in VO2peak was observed after the intervention; however, the HIIT group showed a significant improvement compared with the SBE group (p<0.01). Significant reductions were observed in the levels of insulin resistance, triglyceride, total cholesterol, ALT, and AST in both groups, although high-density lipoprotein levels decreased only in the HIIT group (p<0.01). Further, a significant reduction in low-density lipoprotein level was observed in the training groups (p<0.01), but this decrease was not significant compared with the control group (p>0.01). Conclusion: HIIT and SBE are equally effective in improving health parameters in obese children and adolescents.

• Animal Bioscience
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• v.35 no.1
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• pp.22-28
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• 2022

Objective: Endoplasmic reticulum (ER) stress engages the unfolded protein response (UPR) that serves as an important mechanism for modulating hepatic fatty acid oxidation and lipogenesis. Chronic fasting in mice induced the UPR activation to regulate lipid metabolism. However, there is no direct evidence of whether negative energy balance (NEB) induces ER stress in the liver of cows. This study aimed to elucidate the relationship between the NEB attributed to feed deprivation and ER stress in bovine hepatocytes. Methods: Blood samples and liver biopsy tissues were collected from 6 non-lactating cows before and after their starvation for 48 h. The blood non-esterified fatty acids (NEFA), β-hydroxybutyric acid (BHBA) and glucose level were analyzed. Real-time quantitative polymerase chain reaction and Western blotting were used to explore the regulation of genes associated with UPR and lipid metabolism. Results: The starvation increased the plasma BHBA and NEFA levels and decreased the glucose level. Additionally, the starvation caused significant increases in the mRNA expression level of spliced X-box binding protein 1 (XBP1s) and the protein level of phosphorylated inositol-requiring kinase 1 alpha (p-IRE1α; an upstream protein of XBP1) in the liver. The mRNA expression levels of peroxisome proliferator-activated receptor alpha and its target fatty acid oxidation- and ketogenesis-related genes were significantly upregulated by the starvation-mediated NEB. Furthermore, we found that the mRNA expression levels of lipogenic genes were not significantly changed after starvation. Conclusion: These findings suggest that in the initial stage of NEB in dairy cows, the liver coordinates an adaptive response by activating the IRE1 arm of the UPR to enhance ketogenesis, thereby avoiding a fatty liver status.

• The Korea Journal of Herbology
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• v.33 no.5
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• pp.1-8
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• 2018

Objectives : The aim of this study is to investigate the preventive effect of Puerariae Flos ethanol extract (PE) on methionin and choline deficient (MCD)-diet-induced Nonalcoholic fatty liver disease (NAFLD) in C57BL/6J mice. Methods : In the in vivo experiments, C57BL/6J mice were divided into 4 groups; Normal group, Control group, MCD+PE 100 group, and MCD+PE 300 group. After 4 weeks, body weight, liver weight, biochemical parameters for liver function test, histological changes, reverse transcription polymerase chain reaction (RT-PCR), and Western blot were assessed. Results : Mice lost body weight with the MCD-diet and the MCD+PE 100 group and MCD+PE 300 groups lost less than the control group, though showed no statistical significance. Liver weights were decreased by the MCD diet, but MCD+PE 300 groups were increased significantly. In the liver function test, all the values were decreased with the MCD-diet, MCD+PE 100 group and MCD+PE 300 groups were increased significance. In histological findings of the livers, MCD-diet induced severe fatty accumulation in the livers, but this fatty change was reduced in the MCD+PE 100 group and MCD+PE 300 groups was inhibited respectively. In lipid accumulation factors (such as SREBP-1c, $C/EBP{\alpha}$, PPAR-${\gamma}$), MCD+PE 100 group and MCD+PE 300 groups showed inhibitory effect on liver lipogenesis by reducing associated gene expressions caused by MCD diet. Conclusions : We were able to know that Puerariae Flos ethanol extract (PE) shown hepatoprotective effects via a decrease on the hepatic lipogenesis factors in the experimental NAFLD Models.

• 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.

• Asian-Australasian Journal of Animal Sciences
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• v.24 no.9
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• pp.1274-1281
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• 2011

Dietary protein restriction affects lipid metabolism in rats. This study was performed to determine the effect of a low protein diet on hepatic lipid metabolism and insulin sensitivity in growing male rats. Growing rats were fed either a control 20% protein diet or an 8% low protein diet. Feeding a low protein diet for four weeks from 8 weeks of age induced a fatty liver. Expression of acetyl-CoA carboxylase, a key lipogenic enzyme, was increased in rats fed a low protein diet. Feeding a low protein diet decreased very low density lipoprotein (VLDL) secretion without statistical significance. Feeding a low protein diet down-regulated protein expression of microsomal triglyceride transfer protein, an important enzyme of VLDL secretion. Feeding a low protein diet increased serum adiponectin levels. We performed glucose tolerance test (GTT) and insulin tolerance test (ITT). Both GTT and ITT were increased in protein-restricted growing rats. Our results demonstrate that dietary protein restriction increases insulin sensitivity and that this could be due to low-protein diet-mediated metabolic adaptation. In addition, increased adiponectin levels may influences insulin sensitivity. In conclusion, dietary protein restriction induces a fatty liver. Both increased lipogenesis and decreased VLDL secretion has contributed to this metabolic changes. In addition, insulin resistance was not associated with fatty liver induced by protein restriction.

• 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.