Fig. 3: LBP binds with unsaturated TG to prevent against lipid peroxidation.

a A pie chart showing the difference in lipid composition between WT (n = 3) and LBPKI/KI (n = 3) mice liver after 16 weeks of HFD. b Analysis of chain length of differential TGs in (a). Shown are means ± s.e.m., (n = 3, biologically independent). c Analysis of saturation of differential TGs in (a). Shown are means ± s.e.m., (n = 3, biologically independent). d Targeted quantitative lipidomics illustrating the ratio of fatty acid content in the liver tissue of LBPKI/KI and LBP−/− groups compared to the WT group. e Confocal microscopy images show co-stained lipid droplets (Bodipy 493/503, green) formed by PA and LBP (violet), with DAPI (blue) counterstaining. Line graphs represent relative intensity quantification of the area indicated by the red arrow. Scale bars: 5 µm for the main image, 1 µm for the magnified area. Experiments were independently repeated three times with consistent results. f Kinetic line graph illustrating the results of Seahorse analyses, indicating that overexpression of LBP leads to an increase in FAO rate.Shown are means ± s.d. (n = 4, biologically independent). g Analysis of basal, maximal OCR, and ATP-linked respiration data from the experiment in (f).Shown are means ± s.d., 2way ANOVA (n = 4, biologically independent). h A pie chart illustrates the changes in lipid composition bound to LBP before and after 3 h 500 uM H2O2 stimulation. i Analysis of chain length of differential TGs in (h). Shown are means ± s.e.m., (n = 3, biologically independent). j Analysis of saturation of differential TGs in (h). Shown are means ± s.e.m., (n = 3, biologically independent). k LBP lipid overlay assay using purified LBP with non-treatment or 1 h 1 mM H2O2 treatment lipid-bound membranes. l Dose-response curves for determination of Kd for the binding of LBP to tridocosahexaenoin using a labeled MST assay. Shown are means ± s.d., (n = 3, biologically independent).