Fig. 2: The localization of LBP to LDs drives hepatic steatosis.
a Hepatic TG content of WT mice under NT, 24 h fasting, or LPS-treatment (5 mg/kg, i.p.) for 24 h. Shown are means ± s.d., one-way ANOVA (n = 3, biologically independent). b Representative bright-field microscope image showing separated LDs from the same treatment as described in (a), scale bar = 10 μm. Experiments was conducted with three biological replicates and produced similar results. c TEM and Oil red O staining of LDs in the livers of WT and LBPKI/KI mice with 16-week HFD. TEM scale bar = 2 μm, Yellow arrows indicate LDs. Oil red scale bar = 20 μm. Experiments was conducted with three biological replicates and produced similar results. d Primary hepatocytes isolated from WT, LBP−/−, LBPKI/KI mice treated with Bodipy C12 (orange) for 16 h and co-stained with PLIN2 (violet) and LBP (blue). Scale bar = 2 μm. Experiments repeated two times independently with similar results. e Hepatic TG content of LBP−/− mice overexpressing GFP/LBP-GFP. Shown are means ± s.d., two-tailed unpaired t-test (n = 6, biologically independent). f Representative confocal imaging of LDs separation from liver in (e). Scale bar = 10 μm. g Representative TEM images of control-APEX2 and LBP-APEX2 morphology, scale bar = 500 nm. Experiments repeated two times independently with similar results.
