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.

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.

Loss of function of membrane-bound O-acyltransferase 7 (MBOAT7), but not transmembrane channel-like 4 (TMC4), promotes hepatic steatosis.

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.

Circadian neutrophil infiltration in the liver modulates liver clock-gene expression and daily hepatic metabolism through the secretion of elastase and activation of JNK-FGF21-Bmal1 axis in the hepatocyte.

The hepatic endocannabinoid/CB₁R system controls the soluble leptin receptor’s expression and/or subsequent release by Trib3-induced regulation of C/EBP homologous protein levels in hepatocytes to affect leptin signaling in the liver.

Store operated calcium entry is defective in hepatocytes of obese mice, and restoring this process is sufficient to improve glucose metabolism.

Genetic mouse models show that hepatic NIK and IKKα inhibit hepatocyte proliferation and liver regeneration in part by inhibiting the JAK2/STAT3 pathway.

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