The Ameliorating Effects of n-3 Polyunsaturated Fatty Acids on Liver Steatosis Induced by a High-Fat Methionine Choline-Deficient Diet in Mice.

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is associated with abnormalities of liver lipid metabolism. On the contrary, a diet enriched with n-3 polyunsaturated fatty acids (n-3-PUFAs) has been reported to ameliorate the progression of NAFLD. The aim of our study was to investigate the impact of dietary n-3-PUFA enrichment on the development of NAFLD and liver lipidome.

Serum concentration of taurochenodeoxycholic acid predicts clinically significant portal hypertension.

Background & Aims: Severity of portal hypertension is usually quantified by measuring the hepatic venous pressure gradient (HVPG). However, due to its invasiveness, alternative markers are being sought. Bile acids (BA), being synthesized, metabolized, and transported by the liver, seem to have the potential to serve as endogenous markers.

An overview of current therapy options of non-alcoholic fatty liver disease.

Finding an effective treatment of non-alcoholic fatty liver disease (NAFLD) remains one of main challenges in hepatological research for the 21st century, since there is no such a treatment yet. Lifestyle modifications leading to weight reduction are cheap and effective, however only a fraction of patients reaches significant weight loss goals. Current pharmacological treatment of NAFLD comprises screening and therapy of metabolic syndrome components and minimizing of alcohol intake.

Diagnosis of non-alcoholic fatty liver disease and its active screening in risk groups.

Non-alcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease in developed countries, where it affects up to a quarter of the population. The groups at most risk are diabetics, obese and patients with dyslipidemia, i. e.

Liver tests.

Liver function tests are among the most determined biochemical parameters, and it is essential that their interpretation is always performed correctly. The presence of liver disease is indicated not only by the well-known basic panel of liver function tests (bilirubin, ALT, AST, GGT and ALP), but also by other biochemical parameters, especially albumin, INR and platelet count. The latter analytes are often overlooked, as is the fact that normal values in the baseline liver test panel do not yet rule out advanced chronic liver disease - liver fibrosis or cirrhosis.

Metabolic subtypes of patients with NAFLD exhibit distinctive cardiovascular risk profiles.

Background And Aims: We previously identified subsets of patients with NAFLD with different metabolic phenotypes. Here we align metabolomic signatures with cardiovascular disease (CVD) and genetic risk factors.

Approach And Results: We analyzed serum metabolome from 1154 individuals with biopsy-proven NAFLD, and from four mouse models of NAFLD with impaired VLDL-triglyceride (TG) secretion, and one with normal VLDL-TG secretion.

Effect of Omega-3 Polyunsaturated Fatty Acids on Lipid Metabolism in Patients With Metabolic Syndrome and NAFLD.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. n-3 polyunsaturated fatty acids (n-3-PUFAs) have been reported to ameliorate the progression of NAFLD in experimental studies; however, clinical trials have yielded contradictory results. The aim of our study was to assess the effects of n-3-PUFA administration on lipid metabolism and the progression of NAFLD in patients with metabolic syndrome.

Association of Serum Bilirubin and Functional Variants of Heme Oxygenase 1 and Bilirubin UDP-Glucuronosyl Transferase Genes in Czech Adult Patients with Non-Alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder worldwide. The aim of our study was to assess the role of bilirubin, and the heme oxygenase 1 () and bilirubin UDP-glucuronosyl transferase () promoter gene variants, which are involved in bilirubin homeostasis, in the NAFLD development in adult patients. The study was performed on 84 patients with NAFLD and 103 age/sex-matched controls.

The Effect of Mycotoxins and Silymarin on Liver Lipidome of Mice with Non-Alcoholic Fatty Liver Disease.

Milk thistle-based dietary supplements have become increasingly popular. The extract from milk thistle () is often used for the treatment of liver diseases because of the presence of its active component, silymarin. However, the co-occurrence of toxic mycotoxins in these preparations is quite frequent as well.

Clinically silent LINE 1 insertion in the PNPLA3 gene may impede genotyping of the p.I148M variant.

The patatin-like phospholipase domain containing 3 (PNPLA3) gene (viz. its I148M variant) is one of the key players in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). We have identified a novel insertion/deletion variant of 1114 bp, localized in the second intron of the PNPLA3 gene, which corresponds to the 3' terminal sequence of the long-interspersed element (LINE-1).

Non-alcoholic fatty liver disease - how to effectively fight the nowadays most common liver disease?

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease nowadays. It is referred to as liver manifestation of metabolic syndrome. Given the growing incidence of diabetes and obesity, we can confidently say that we will be, or even are facing, a NAFLD pandemic in the near future.

Acute responses of hepatic fat content to consuming fat, glucose and fructose alone and in combination in non-obese non-diabetic individuals with non-alcoholic fatty liver disease.

We have recently demonstrated that a high-fat load can induce immediate increase in hepatic fat content (HFC) and that such an effect can be modified differently by co-administration of fructose or glucose in healthy subjects. Therefore, we addressed the question how consumption of these nutrients affects changes in HFC in subjects with non-alcoholic fatty liver disease (NAFLD). Eight male non-obese non-diabetic patients with NAFLD underwent 6 experiments each lasting 8 hours: 1.

[Liver fibrosis].

Liver fibrosis is the excessive deposition of extracellular matrix in liver tissue resulting in structural and functional liver changes. The basis for these changes is the imbalance between fibrogenesis and fibrolysis, which arises in response to chronic liver damage, regardless of its aetiology. Advanced liver fibrosis leads to cirrhosis with its possible complications - portal hypertension, hepatocellular carcinoma, and liver failure.

Increased Susceptibility of Cattle to Intranasal RVFV Infection.

Rift Valley Fever virus (RVFV) is a zoonotic mosquito-borne virus that belongs to the Phenuiviridae family. Infections in animal herds cause abortion storms, high mortality rates in neonates, and mild to severe symptoms. Infected animals can also transmit the virus to people, particularly people who live or work in close contact with livestock.

Osteopontin - A potential biomarker of advanced liver disease.

Cirrhosis is a primary cause of liver-related mortality and morbidity. The basic process driving chronic liver disease to cirrhosis is accelerated fibrogenesis. Although the pathogenesis of liver cirrhosis is a multifactorial process, the essential step in the evolution of liver fibrosis is the activation of hepatic stellate cells, which are the main source of collagen produced in the extracellular matrix.

RVFV Infection in Goats by Different Routes of Inoculation.

Rift Valley fever virus (RVFV) is a zoonotic arbovirus of the Phenuiviridae family. Infection causes abortions in pregnant animals, high mortality in neonate animals, and mild to severe symptoms in both people and animals. There is currently an ongoing effort to produce safe and efficacious veterinary vaccines against RVFV in livestock to protect against both primary infection in animals and zoonotic infections in people.

Heme Oxygenase-1 May Affect Cell Signalling via Modulation of Ganglioside Composition.

Heme oxygenase 1 (Hmox1), a ubiquitous enzyme degrading heme to carbon monoxide, iron, and biliverdin, is one of the cytoprotective enzymes induced in response to a variety of stimuli, including cellular oxidative stress. Gangliosides, sialic acid-containing glycosphingolipids expressed in all cells, are involved in cell recognition, signalling, and membrane stabilization. Their expression is often altered under many pathological and physiological conditions including cell death, proliferation, and differentiation.

Changes in transcription pattern lead to a marked decrease in COX, CS and SQR activity after the developmental point of the 22(nd) gestational week.

Tissue differentiation and proliferation throughout fetal development interconnect with changes in the oxidative phosphorylation system (OXPHOS) on the cellular level. Reevaluation of the expression data revealed a significant increase in COX4 and MTATP6 liver transcription levels after the 22(nd) gestational week (GW) which inspired us to characterize its functional impact. Specific activities of cytochrome c oxidase (COX), citrate synthase (CS), succinate-coenzyme Q reductase (SQR) and mtDNA determined by spectrophotometry and RT-PCR were studied in a set of 25 liver and 18 skeletal muscle samples at 13(th) to 29(th) GW.

DNA vaccination protects mice against Zika virus-induced damage to the testes.

Zika virus (ZIKV) is an emerging pathogen causally associated with serious sequelae in fetuses, inducing fetal microcephaly and other neurodevelopment defects. ZIKV is primarily transmitted by mosquitoes, but can persist in human semen and sperm, and sexual transmission has been documented. Moreover, exposure of type-I interferon knockout mice to ZIKV results in severe damage to the testes, epididymis and sperm.

Changes in Liver Ganglioside Metabolism in Obstructive Cholestasis - the Role of Oxidative Stress.

Bile acids have been implicated in cholestatic liver damage, primarily due to their detergent effect on membranes and induction of oxidative stress. Gangliosides can counteract these harmful effects by increasing the rigidity of the cytoplasmic membrane. Induction of haem oxygenase (HMOX) has been shown to protect the liver from increased oxidative stress.

Use of non-invasive parameters of non-alcoholic steatohepatitis and liver fibrosis in daily practice--an exploratory case-control study.

Background: Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of a metabolic syndrome. To date, liver biopsy has been the gold standard used to differentiate between simple steatosis and steatohepatitis/fibrosis. Our aim was to compare the relevance of serum non-invasive parameters and scoring systems in the staging of liver fibrosis and non-alcoholic steatohepatitis (NASH) in patients with NAFLD.

The effect of heme oxygenase on ganglioside redistribution within hepatocytes in experimental estrogen-induced cholestasis.

Cholestasis is characterized by the elevation of serum total bile acids (TBA), which leads to the production of both free radicals and oxidative stress. Although they do not share the same mechanisms, membrane glycosphingolipids (GSL) and the antioxidant enzyme heme oxygenase-1 (HMOX1) both act against the pro-oxidative effect of TBA. The aim of the study was to assess the role of HMOX on GSL redistribution and composition within hepatocytes in the rat model of estrogen-induced cholestasis.

Histochemical detection of GM1 ganglioside using cholera toxin-B subunit. Evaluation of critical factors optimal for in situ detection with special emphasis to acetone pre-extraction.

A comparison of histochemical detection of GM1 ganglioside in cryostat sections using cholera toxin B-subunit after fixation with 4% formaldehyde and dry acetone gave tissue-dependent results. In the liver no pre-treatment showed detectable differences related to GM1 reaction products, while studies in the brain showed the superiority of acetone pre-extraction (followed by formaldehyde), which yielded sharper images compared with the diffuse, blurred staining pattern associated with formaldehyde. Therefore, the aim of our study was to define the optimal conditions for the GM1 detection using cholera toxin B-subunit.