Search results for "Fatty Liver"

Sox17 regulates liver lipid metabolism and adaptation to fasting.

2014

Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is …

Fatty liver indexandhepatic steatosis index for prediction ofnon-alcoholic fatty liver disease in type 1 diabetes

2017

Background and Aim Little is known about the diagnostic value of hepatic steatosis index (HSI) and fatty liver index (FLI), as well as their link to metabolic syndrome in type 1 diabetes mellitus. We have screened the effectiveness of FLI and HSI in an observational pilot study of 40 patients with type 1 diabetes. Methods FLI and HSI were calculated for 201 patients with type 1 diabetes. Forty patients with FLI/HSI values corresponding to different risk of liver steatosis were invited for liver magnetic resonance study. In-phase/opposed-phase technique of magnetic resonance was used. Accuracy of indices was assessed from the area under the receiver operating characteristic curve. Results Tw…

A targeted apoB38.9 mutation in mice is associated with reduced hepatic cholesterol synthesis and enhanced lipid peroxidation.

2006

Familial hypobetalipoproteinemia (FHBL) due to truncation-specifying mutations of apolipoprotein B (apoB), which impair hepatic lipid export in very low-density lipoprotein (VLDL) particles, is associated with fatty liver. In an FHBL-like mouse with the apoB38.9 mutation, fatty liver develops despite reduced hepatic fatty acid synthesis. However, hepatic cholesterol contents in apoB38.9 mice are normal. We found that cholesterogenic enzymes (3-hydroxy-3-methylglutaryl-coenzyme A reductase, sterol-C5-desaturase, and 7-dehydrocholesterol reductase) were consistently downregulated in two separate expression-profiling experiments using a total of 19 mice ( n = 7 each for apob+/+and apob+/38.9, …

Former male elite athletes have better metabolic health in late life than their controls

2015

Elite-class athletes have longer life expectancy and lower risk for chronic noncommunicable diseases possibly because of physically active and healthier lifestyle. In this study, we assessed former male Finnish elite-class athletes' (n = 392) and their matched controls' (n = 207) body composition, and risk for the metabolic syndrome (MS) and nonalcoholic fatty liver disease (NAFLD) in later life. Compared with the controls, the former athletes had lower body fat percentage (24.8% vs 26.0%, P = 0.021), lower risk for MS [odds ratio (OR) 0.57, 95% confidence interval (CI) 0.40-0.81], and NAFLD (OR 0.61, 95% CI 0.42-0.88). High volume of current leisure-time physical activity (LTPA) was associ…

HEPATIC EXPRESSION OF CYCLOOXYGENASE-2 IN NON-ALCOHOLIC FATTY LIVER DISEASE

2008

Baseline patient characteristics of the German multicentric prospective real-world NAFLD cohort: The Fatty Liver Assessment in Germany (FLAG) study

2019

Focal hepatic intrinsically hyperattenuating lesions at unenhanced CT: Not always calcifications.

2021

Due to the growing use of CT, there has been an increase in the frequency of detecting focal liver lesions. Intrinsically hyperattenuating hepatic lesions or pseudolesions are not uncommon at unenhanced CT. Hyperattenuating hepatic lesions can be divided into non-calcified and calcified. Causes of intrinsic hyperattenuation include hemorrhage, thrombosis, and calcifications. Focal liver lesions can show hyperattenuation on unenhanced CT in case of severe liver steatosis. Recognition of etiologies associated with hyperattenuation on unenhanced CT can help the radiologist in characterizing focal liver lesions and pseudolesions. In this paper, we describe the spectrum of intrinsically hyperatt…

Presence of the MBOAT7 rs641738 variant might enhance liver fibrosis in patients with fatty liver: analysis of the German NAFLD CSG cohort

2016

The Cost of Non-Alcoholic Steatohepatitis (NASH) in Europe and USA: The GAIN Study

2019

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders. The progressive form of NAFLD, non-alcoholic steatohepatitis (NASH), leads to cirrhosis in a proportion of patients and so is associated with a substantial socio-economic burden which, coupled with a steadily rising prevalence, is becoming a growing public health challenge. The Global Assessment of the Impact of NASH (GAIN) study is a socioeconomic, prevalence-based burden of illness study across Europe (France, Germany, Italy, Spain and the United Kingdom) and the United States to determine the socio-economic burden of NASH in the real-world. Methods: GAIN was a retrospective, cross-sec…

Biochemical biomarkers of NAFLD/NASH

2020

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the Western world and the global epidemics of obesity and type 2 diabetes have led to a dramatic increase of its prevalence and incidence. Among NAFLD patients, those with nonalcoholic steatohepatitis (NASH) have a double risk of fibrosis progression, that is the main driver toward the evolution in cirrhosis and its complications, including hepatocellular carcinoma and hepatic decompensation. Furthermore, patients with NAFLD are also at risk for cardiovascular diseases and extrahepatic malignancies, that represent the first and the second cause of death, respectively. The availability of non-invasi…