Background & Aims Innate immune activation has been postulated as a central mechanism
for disease progression from hepatic steatosis to steatohepatitis in obesity-related fatty liver
disease. Arginase 2 competes with inducible nitric oxide synthase (iNOS) for its substrate
and the balance between these two enzymes plays a crucial role in regulating immune
responses and macrophage activation. Our aim was to test the hypothesis that arginase 2
deficiency in mice favours progression from isolated hepatic steatosis, induced by high fat …