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Molecular Pathogenesis of Liver Steatosis Induced by Hepatitis C Virus

. Depla M, d’Alteroche L, Le Gouge A, Moreau A, Hourioux C, Meunier JC, et al. Viral sequence variation in chronic carriers of hepatitis C virus has a low impact on liver steatosis. PLoS One 2012;7(3):e33749. 7. Ivanov AV, Smirnova OA, Ivanova ON, Masalova OV, Kochetkov SN, Isaguliants MG. Hepatitis C virus proteins activate NRF2/ ARE pathway by distinct ROS-dependent and independent mechanisms in HUH7 cells. PLoS One 2011;6:e24957. 8. Tanaka N, Moriya K, Kiyosawa K, Koike K, Gonzalez FJ, Aoyama T. PPARalpha activation is essential for

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Influence of Non-Oxidised and Oxidised Rapeseed Oil Consumption on Liver Metabolism Pathways and Non-Alcoholic Steatohepatitis Development in Rabbits

Abstract

For 24 weeks, rabbits were fed feed containing non-oxidised or oxidised rapeseed oil. At the beginning of the experiment and every six weeks the rabbits were weighed and blood was taken. After the experiment was completed, their liver was dissected for biochemical and histological examinations. The activity of alanine aminotransferase, aspartate aminotrasferase, glutamate dehydrogenase, sorbitol dehydrogenase, and aldolase in blood plasma and liver were determined. Enzymes of the protein and liver metabolic pathways were determined using kinetic and spectrophotometric methods. The content of fatty acids was determined by means of fatty acid methyl ester concentration measurement using gas chromatography. It was found that the applied diet with oxidised rapeseed oil caused the development of slight liver steatosis and disturbances in the activity of enzymes involved in the liver pathways, despite the fact that it was a balanced diet, and differed only in the ratio of saturated to unsaturated fatty acids. The obtained results indicate that more profound oil oxidation and its increased supply in diet may result in the development of liver steatosis.

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Pathological Alterations in Hepatocytes of Dairy Cows With a Tendency to Emaciation and Fattening

Abstract

The aim of this study was to demonstrate the histochemical and histopathological alterations in the livers of cows with a tendency to become emaciated (body condition score - BCS1 and 2) and a tendency to become fattened (BCS4 and 5) in comparison to the cows of average body condition (BCS3) presented as a control. The histochemical analysis (PAS reaction) showed that the influence of emaciation and fattening in our study was manifested by a decreased occurrence of glycogen and a decreased level of the PAS-positive matter in the hepatocytes of dairy cows with BCS1, 2, 4 and 5. An abundant accumulation of lipids in the form of large lipid droplets, liposomes and lipoproteins observed in the hepatocytes of emaciated and fattened (BCS1 and 5) cows may be related to moderate-severe steatosis. These observations suggest a relationship between liver steatosis and the occurrence of lipoproteins in cows with a tendency toward emaciation and fattening.

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Physical activity as a protective factor against development of liver steatosis in patients infected with hepatitis C

Summary

Study aim: Was to verify whether the regular practice of physical activity promotes some protective factor against the develop­ment of LS in patients infected with hepatitis C virus (HCV). Materials and method: Clinical data were obtained through medical records available at the Pernambuco Liver Institute. Physi­cal activity levels were obtained through the International Physical Activity Questionnaire (IPAQ) short form to classify the patients according to the guidelines of the American College of Sports Medicine (ACSM). Results: The sample consisted of patients of both genders, over 18 years of age, who had positive anti-HCV, HCV-RNA and confirmatory tests for presence or absence of liver steatosis. 126 patients were included in the study. Patients with liver steatosis (G1) were more frequently male (57%) compared to patients without liver steatosis (G2) (p = 0.02). Physical activity analysis showed significant differences for GGT (p = 0.04), HDL (p = 0.04), AF (p = 0.02), viral genotype 3 (p = 0.04) and waist-to-hip ratio (p = 0.01) in anthropometric data. Correlation analysis showed a significant difference for GGT (r = -0.23; p = 0.01) and total bilirubin (BT) (r = -0.22; p = 0.01). Conclusions: Regular practice of physical activity generates a protective factor against the development of LS in patients in­fected by the hepatitis C virus and it is associated with the maintenance of variables related to hepatic and biochemical damage in patients infected with HCV.

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ST2 Deficiency Ameliorates High Fat Diet-Induced Liver Steatosis In BALB/c Mice

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity, but the molecular mechanisms of liver steatosis and its progression to non-alcoholic steatohepatitis and fibrosis are incompletely understood. Immune reactivity plays an important role in the pathogenesis of NAFLD. The IL-33/ST2 axis has a protective role in adiposity and atherosclerosis, but its role in obesity-associated metabolic disorders requires further clarification. To investigate the unresolved role of IL-33/ST2 signalling in NAFLD, we used ST2-deficient (ST2-/-) and wild type (WT) BALB/c mice maintained on a high-fat diet (HFD) for 24 weeks. HFD-fed ST2-/- mice exhibited increased weight gain, visceral adipose tissue weight and triglyceridaemia and decreased liver weight compared with diet-matched WT mice. Compared with WT mice on an HFD, ST2 deletion significantly reduced hepatic steatosis, liver inflammation and fibrosis and downregulated the expression of genes related to lipid metabolism in the liver. The frequency of innate immune cells in the liver, including CD68+ macrophages and CD11c+ dendritic cells, was lower in HFD-fed ST2-/- mice, accompanied by lower TNFα serum levels compared with diet-matched WT mice. Less collagen deposition in the livers of ST2-/- mice on an HFD was associated with lower numbers of profibrotic CD11b+Ly6clow monocytes and CD4+IL-17+ T cells in the liver, lower hepatic gene expression of procollagen, IL-33 and IL-13, and lower serum levels of IL-33 and IL-13 compared with diet-matched WT mice.

Our findings suggest that the IL-33/ST2 axis may have a complex role in obesity-associated metabolic disorders. Although it is protective in HFD-induced adiposity, the IL-33/ST2 pathway promotes hepatic steatosis, inflammation and fibrosis.

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Noninvasive Markers of Improvement of Liver Steatosis Achieved by Weight Reduction in Patients with Nonalcoholic Fatty Liver Disease

Abstract

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance and metabolic syndrome, which are linked to obesity. The aim of the study was to assess if weight reduction through 12 months of lifestyle intervention and exercise would lead to improvement of steatosis.

Methods. In a prospective observational study 86 overweight subjects (51 men, 35 women) with steatosis were recruited, after excluding other etiologies. Patients were assigned a caloric goal and a daily fat goal. Physical activity focused on moderate-intensity activities. Blood samples (biochemistry, HOMA-IR, cytokine levels, steatotest) were collected at entry and months 6 and 12. All subjects underwent abdominal CT scan before commencement and after 12 months to assess visceral and subcutaneous adipose tissue (VAT/SAT) area.

Results. After 12 months baseline descriptive characteristics (weight, BMI, waist circumference) decreased significantly. Biochemical parameters that decreased significantly were: GGT (40.0 ± 18.0 vs 31.1 ± 13; p = 0.01), ALT (58.5 ± 23.5 vs 32,7 ± 14.8; p = 0.001), cholesterol (236.4 ± 54.8 vs 204.8 ± 91; p = 0.05), LDL (160.1 ± 47.4 vs 125.3 ± 40; p = 0.05) and HOMA-R (4.86 ± 0.63 vs 3 ± 0.41; p = 0.018). Steatotest improved significantly (0.68 ± 0.16 vs 0.38 ± 0.14; p = 0.02). Modification of adipocytokines was significant for leptin (p = 0.018) and adiponectin (p = 0.003). Factors associated with regression of steatosis were weight, BMI, ALT, waist circumference, GGT, HOMA, leptin, VAT and steatotest. Multivariate logistic regression showed the following factors related to improved steatosis: BMI < 25 kg/m2, ALT < 42 U/L, leptin < 10.5 ng/ml and adiponectin > 8.4 μg/ml.

Conclusions. Overweight persons who achieve significant reductions in body weight through 12 months of physical activity and low caloric diet can decrease liver fat, VAT and SAT. Even in those with minimal weight loss ALT levels, steatosis, adipokines and cardiovascular risk factors improved.

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Insulin Resistance in Liver Diseases

Insulin Resistance in Liver Diseases

Present report gives a brief and consolidated review of insulin resistance developed in chronic liver diseases. Insulin resistance remains an important feature of chronic liver diseases and progresses disease towards fibrogenesis. Of hepatitis viral infections, hepatitis C virus (HCV) was reported to have a significant role in inducing insulin resistance. Both viral particles as such, as well its structural components induce insulin resistance. Hepatitis C virus core protein, specially, causes insulin resistance via its direct action on insulin signaling cascade as well as by inducing over expression of certain cytokines including TNF-α. Insulin resistance has a direct relation with liver steatosis and oxidative stress. Both steatosis and oxidative stress enhances insulin resistance and vice-a-versa. Insulin resistance has widespread implications on metabolism and needs its correction before planning therapeutic regimen in liver diseases.

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Diabetes Mellitus, Obesity and Underlying Non Alcoholic Fatty Liver Disease - Independent Risk Factors for Hepatocellular Carcinoma

Abstract

Background and Aims. Hepatocellular carcinoma (HCC) is one of the most common malignancies. Obesity, together with the underlying liver steatosis, has received increased attention as a risk factor for HCC. Diabetes Mellitus (DM) is also reported to be associated with HCC. We aimed to estimate the risk of HCC in obese and diabetic patients. Material and method. We prospectively analyzed 414 obese and diabetic patients, over a period of 5 years. We evaluated all patients using screening methods such as abdominal ultrasound and serum alpha-fetoprotein every 6 month, in order to detect HCC occurrence. Kaplan-Meier analysis estimated the cumulative incidence of HCC. Univariate and multivariate Cox regression analysis assessed the association between HCC and obesity. Results. Median follow-up was 4.3 years. 11 from 77 cirrhotic obese patients, and 18 from 150 non-cirrhotic obese patients developed HCC (p=ns). 7 from 51 patients with DM and cirrhosis, and 14 from 136 non-cirrhotic patients with DM developed HCC (p=ns). The cumulative incidence of HCC was 2.8%, respectively 2.6%, in cirrhotic patients with obesity or DM, compared with 2.2%, respectively 2.0%, in non-cirrhotic patients with obesity or DM (p=ns). Conclusion. Obesity and DM, along with nonalcoholic fatty liver disease (NAFLD), seems to be independent risk factors for HCC occurrence.

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Polyphenols treatment in patients with nonalcoholic fatty liver disease

the progression from simple fat accumulation to NASH.[ 20 ] Several evidences in vitro , pre-clinical and emerging clinical trials reported beneficial effects on liver steatosis and its pathogenic and clinical setting.[ 20 - 23 ] Few clinical studies were focused on the polyphenols use in NAFLD patients. Three were undertaken with 500 mg and 600 mg resveratrol daily for 12 weeks, or 3000 mg daily for 8 weeks respectively.[ 24 - 26 ] Other two studies were carried out using 150 mg polyphenols (1.43% of flavonoids, 2.5% anthocyanins and 1.7% phenolic acid) extract

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Adipokines, insulin resistance, hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis

. Liver fibrosis is not associated with steatosis but with necroinflammation in French patients with chronic hepatitis C. Gut. 2003; 52:1638-43. 19. Testino G, Sumberaz A. Liver steatosis and antiviral therapy in chronic hepatitis C. Liver Int. 2007; 27:287. 20. Sanyal AJ, Contos MJ, Sterling RK, Luketic VA, Shiffman ML, Stravitz RT, et al. Nonalcoholic fatty liver disease in patients with hepatitis C is associated with features of the metabolic syndrome. Am J Gastroenterol. 2003; 98:2064-71. 21. Gordon A, McLean CA

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