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.

Antibody-mediated neutralisation of Gremlin-1 was ineffective in treating fibrosis in metabolic dysfunction-associated steatohepatitits, likely due to low hepatic expression in a subset of myofibroblasts and redundant Gremlin-1 signalling.

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

MBOAT7 loss of function in hepatocytes contributes to ethanol-induced liver injury, offering crucial insights into the dysregulated lipid metabolism and impaired autophagy associated with advanced liver disease.

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

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.

The size of subcutaneous, but not visceral, fat depots is dependent on the number of embryonic adipocyte progenitors.