B cell lymphoma 6 (BCL6) represses fasting gene expression by opposing peroxisome proliferator-activated receptor alpha (PPARa) activity at enhancers, and its ablation protects against steatosis by enhancing fatty acid catabolism.

The Hedgehog signalling pathway is a master regulator of lipid metabolic processes and their zonation in the adult liver of mice and humans.

Identifying xanthohumol and its derivatives as PPARγ anatagonists provides new insight into how natural compounds beneficially treat obesity and metabolic syndrome, and provide new compounds for therapeutic development.

Ablation of the G-protein-coupled receptor C3aR1 specifically on macrophages or Kupffer cells does not alter the course of metabolic dysfunction-associated steatotic liver disease in a dietary mouse model.

A system genetics approach reveals a unique molecular signature of non-alcoholic fatty liver disease in mice and identifies novel genetic factors affecting hepatic steatosis.

A microbiome metabolite alleviates liver steatosis and inflammation, and shows its potential as a therapeutic modality for non-alcoholic fatty liver disease.

Loss of hepatic Cdk1 leads to oxidative stress, increased fatty acids in blood, and hyperinsulinemia, which resulted in insulin resistance and hepatic steatosis, similar as in diabetes.

Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

LncRNA-Snhg3 regulates lipid metabolism by affecting chromatin accessibility which indicates that lncRNA-mediated epigenetic modification has a crucial role in the pathology of metabolic dysfunction-associated fatty liver disease.

Proteomic-based discovery of a novel mechanism of action affording anti-steatotic properties of itaconate through stabilization of fatty acid oxidation enzyme protein abundance.