Quantitative measurement of ultrasound attenuation and Hepato-Renal Index in Non-Alcoholic Fatty Liver Disease.

Objective: The aim of this study was to non-invasively explore new methods of ultrasound attenuation measurements in livers of patients with Non-Alcoholic-Fatty-Liver-Disease (NAFLD) and to measure the liver tissue elasticity.

Material And Method: Sixteen patients with NAFLD, twelve patients with liver fibrosis and fifteen healthy subjects were included. Echo Levels (ELs) in dB were measured at 2 and 7 cm depths in the right liver to calculate the attenuation.

Combining transient elastography with FIB4 enhances sensitivity in detecting advanced fibrosis of the liver.

Objective: To evaluate the predictive value of transient elastography (TE), easy available biochemical scores and a combination of these to detect advanced liver fibrosis (i.e. fibrosis stage ≥F3) in patients with chronic liver disease of different etiologies.

Fetuin A in nonalcoholic fatty liver disease: in vivo and in vitro studies.

Objective: Fetuin A has been associated with insulin resistance and the metabolic syndrome. We therefore explored the role of fetuin A in nonalcoholic fatty liver disease (NAFLD).

Design: Cross-sectional and intervention studies.

Intracellular nicotinamide phosphoribosyltransferase protects against hepatocyte apoptosis and is down-regulated in nonalcoholic fatty liver disease.

Context: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in Western and non-Western countries, but its pathogenesis is not fully understood.

Objective: Based on the role of nicotinamide phosphoribosyltransferase (NAMPT) in fat and glucose metabolism and cell survival, we hypothesized a role for NAMPT/visfatin in the pathogenesis of NAFLD-related disease.

Design And Setting: We conducted clinical studies at a referral medical center in well-characterized NAFLD patients (n = 58) and healthy controls (n = 27).

Metformin in patients with non-alcoholic fatty liver disease: a randomized, controlled trial.

Objective: The antidiabetic agent metformin is regularly discussed as a promising treatment for non-alcoholic fatty liver disease (NAFLD), which is characterized by insulin resistance. However, the evidence for its beneficial effects is limited, and conflicting reports have been published. The purpose of this study was to conduct a randomized, double-blind, placebo-controlled trial to test whether metformin improves liver histology in patients with non-alcoholic fatty liver disease.

A complex role of activin A in non-alcoholic fatty liver disease.

Objectives: Recent studies suggest that activin A, a member of the transforming growth factor (TGF) superfamily, is involved in the pathogenesis of liver disorders. We sought to explore its possible role in non-alcoholic fatty liver disease (NAFLD).

Methods: Serum levels of activin A and its natural inhibitor, follistatin, were measured in patients with NAFLD (n=70) and in control subjects (n=30).

Gene expression profiles reflect sclerosing cholangitis activity in abcb4 (-/-) mice.

Objective: Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC), a condition that involves differential hepatic transcription of genes governing inflammation, tissue remodelling and fibrosis. The objective of this study was to test the hypothesis that genes involved in the regulation of tissue inflammation and fibrosis display transcription rates that parallel differences in abcb4 (-/-) SC activity. The activity of abcb4 (-/-) SC can be altered through dietary intervention: abcb4 (-/-) mice fed cholic acid (CA) display high SC activity, whereas ursodeoxycholic acid (UDCA)-fed mice display low SC activity.

Multiple inflammatory-, tissue remodelling- and fibrosis genes are differentially transcribed in the livers of Abcb4 (-/ - ) mice harbouring chronic cholangitis.

Objective: Abcb4 (-/-) mice secrete phosphatidylcholine-free, cytotoxic bile and develop chronic cholangitis. The aim of this study was to identify differentially transcribed genes whose products contribute to the liver tissue pathology during this disease.

Material And Methods: Hepatic gene transcription was measured in 3-, 6-, 9- and 20-week-old Abcb4 (-/-) mice (FVB.

Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2.

Background/aims: To elucidate the role of systemic inflammation in nonalcoholic fatty liver disease (NAFLD).

Methods: Serum samples in 47 patients with histologically verified NAFLD (22 with simple steatosis and 25 with nonalcoholic steatohepatitis [NASH]), and in 30 age-, sex- and ethnicity-matched healthy controls, were assessed for (i) general markers of inflammation (C-reactive protein [CRP], tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6), (ii) chemokines (CC-chemokine ligand [CCL] 2/monocyte chemoattractant protein [MCP]-1, CCL19 and CCL21), (iii) adipocytokines related to insulin resistance and inflammation (adiponectin and leptin) and (iv) a marker of oxidative stress (8-isoprostane-F2alpha).

Results: Serum levels of several inflammatory cytokines were increased in NAFLD as compared to controls, and IL-6 (P=0.

Abnormal glucose tolerance is a predictor of steatohepatitis and fibrosis in patients with non-alcoholic fatty liver disease.

Objective: The majority of patients with non-alcoholic fatty liver disease (NAFLD) have simple steatosis. A minority, however, present with non-alcoholic steatohepatitis (NASH), a condition that can lead to advanced fibrosis and cirrhosis. The frequencies of NASH and fibrosis among patients with NAFLD and sustained elevation of liver function tests (LFT) are uncertain.