Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease
By D. H. Ipsen, J. Lykkesfeldt, P. Tveden‐Nyborg. Cellular and Molecular Life Sciences, 2018
1,259 citations recorded by the source corpus.
Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.
Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Epidemiology
View Paper: https://www.semanticscholar.org/paper/03929ae0048c92db1837ff46e0b1d9850e3ffbc2
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Citations in the corpus
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances (2025, positive): “400,405 An inhibition in mitochondrial fusion, especially caused by the down-regulation of Mfn, is closely related to liver diseases due to an impairment in fatty acid oxidation, the TCA cycle, and glycolysis.”
- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, background): “During NAFLD, the impairment of FAO inhibits the activity of PPARα, resulting in hepatic lipid accumulation and inflammation.(296) Liver mitochondria from aged mice produce more ROS and have a greater extent of dysfunction than those from young mice.”