Results 81 to 90 of about 101,002 (279)

Triglyceride peroxidation progression in lipid droplets of hepatocytes in nonalcoholic steatohepatitis

open access: yesRedox Experimental Medicine
Objective: Nonalcoholic steatohepatitis is a chronic liver disease caused by the progression of hepatocellular death and inflammation from simple steatosis. However, the pathogenesis of this disease remains unclear.
Kota Saito   +5 more
doaj   +1 more source

Transcriptional Regulation of Metabolic Pathways via Lipid-Sensing Nuclear Receptors PPARs, FXR, and LXR in NASHSummary

open access: yesCellular and Molecular Gastroenterology and Hepatology, 2021
Nonalcoholic fatty liver disease comprises a wide spectrum of liver injuries from simple steatosis to steatohepatitis and cirrhosis. Nonalcoholic steatohepatitis (NASH) is defined when liver steatosis is associated with inflammation, hepatocyte damage ...
Marica Cariello   +2 more
doaj   +1 more source

Endothelial dysfunction in adolescents and young adults with nonalcoholic liver disease [PDF]

open access: yes, 2019
Nonalcoholic liver disease is a global public health problem that increases cardiovascular morbidity and mortality in these patients. This paper discusses endothelial dysfunction among patients (adolescents and young adults) with nonalcoholic liver ...
Donoiu, Ionuț   +6 more
core   +1 more source

DNA Hydroxymethylation at the Interface of the Environment and Nonalcoholic Fatty Liver Disease. [PDF]

open access: yes, 2019
Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent forms of chronic liver disorders among adults, children, and adolescents, and a growing epidemic, worldwide.
Besaratinia, Ahmad, Tommasi, Stella
core   +1 more source

A Novel CYP2E1 Inhibitor, 4‐Methyl‐5‐Acetylthiazole (Q11), Alleviates Obesity Via Modulating Adipose Inflammation and Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
Obesity involves chronic inflammation and mitochondrial dysfunction. This study identifies cytochrome P450 2E1 (CYP2E1) as a novel inflammatory target in adipose tissue. Its activity increases in obese mice and correlates with inflammation and mitochondrial impairment.
Jinhuan Qiu   +10 more
wiley   +1 more source

Relevant issues in the diagnosis and treatment of nonalcoholic fatty liver disease

open access: yesМедицинский совет, 2015
Nonalcoholic fatty liver disease is a chronic disease uniting steatosis, nonalcoholic steatohepatitis and cirrhosis. Nonalcoholic fatty liver disease is associated with obesity and is a component of metabolic syndrome, thus increasing cardiometabolic ...
E. A. Cherkashina
doaj   +1 more source

Enhancing Hepatic MBOAT7 Expression Does Not Improve Nonalcoholic Steatohepatitis in Mice [PDF]

open access: gold, 2022
Martin C. Sharpe   +11 more
openalex   +1 more source

Immune and Inflammatory Pathways in Non-Alcoholic Steatohepatitis (NASH). An update [PDF]

open access: yes, 2019
Non-alcoholic steatohepatitis (NASH), also known as fatty liver disease (FLD), is a major public health problem. It is considered to be the hepatic manifestation of the metabolic syndrome.
Breaban, Iulia   +10 more
core   +1 more source

Phenotypical heterogeneity linked to adipose tissue dysfunction in patients with type 2 diabetes [PDF]

open access: yes, 2016
Adipose tissue (AT) inflammation leads to increased free fatty acid (FFA) efflux and ectopic fat deposition, but whether AT dysfunction drives selective fat accumulation in specific sites remains unknown.
ANGELICO, Francesco   +12 more
core   +1 more source

OCTN2 Activates a Non‐Canonical Carnitine Metabolic Pathway to Promote MASH‐HCC Progression and Immunotherapy Resistance

open access: yesAdvanced Science, EarlyView.
In non‐MASH‐HCC, L‐carnitine promotes tumor progression primarily through its classical role in enhancing fatty acid oxidation (FAO). However, in MASH‐HCC, where FAO is markedly suppressed, L‐carnitine shifts from this canonical function to serve instead as an intracellular acetyl group buffer.
Chuqi Xia   +11 more
wiley   +1 more source

Home - About - Disclaimer - Privacy