Hepatocyte and stellate cell deletion of liver fatty acid binding protein reveals distinct roles in fibrogenic injury

Liver fatty acid binding protein (L-Fabp) modulates lipid trafficking in enterocytes, hepatocytes, and hepatic stellate cells (HSCs). We examined hepatocyte vs. HSC L-Fabp deletion in hepatic metabolic adaptation and fibrotic injury. Floxed L-Fabp mice were bred to different transgenic Cre mice or injected with adeno-associated virus type 8 (AAV8) Cre and fed diets to promote steatosis and fibrosis or were subjected to either bile duct ligation or CCl4 injury. Albumin-Cre–mediated L-Fabp deletion revealed recombination in hepatocytes and HSCs; these findings were confirmed with 2 other floxed alleles. Glial fibrillary acid protein–Cre and platelet-derived growth factor receptor β-Cre–mediated L-Fabp deletion demonstrated recombination only in HSCs. Mice with albumin promoter–driven Cre recombinase (Alb-Cre)–mediated or AAV8-mediated L-Fabp deletion were protected against food withdrawal–induced steatosis. Mice with Alb-Cre–mediated L-Fabp deletion were protected against high saturated fat–induced steatosi...