Fig. 7: PDI is indispensable for exporting UFA but not SFA esters from liver.

a, b Expression of ApoB, MTP, and PDI in liver lysates from Dex and TM-treated mice (n = 6 biological replicates in each group) were examined by Western blotting using the indicated antibodies (a), and the relative abundance of each protein was quantitated (b). c, d PDI reductase activity (c) and MTP activity (d) of the liver lysates were measured according to the manufacturer’s instructions. n = 4 biological replicates in each group. e, f An in vitro triglyceride transfer assay was performed to measure the SFA (1,3-diolein, 2-NBD-X glycerol ester, DOG-NBD) and UFA (1,3-distearin, 2-NBD-X glycerol ester, DSG-NBD) ester transfer activity of PDI-MTPs. Five μl of acceptor vesicles, 5 μl of donor vesicles containing DSG-BND (e) or DOG-NBD (f), 10 μl of 1% BSA, and 80 μl (50 μg) of liver lysate from WT or PDI-KO mice were added to the wells of a 96-well plate in triplicate. The fluorescence was quantified every minute for 2 h at λex of 463 nm and λem of 536 nm. n = 3 biological replicates in each group. The lines and error bars represent means ± SEM. Source data are provided as a Source Data file. g Schematic diagram of the differential transport mechanism of UFA and SFA esters in hepatocytes under PDI-deficient conditions. MTP microsomal triglyceride transfer protein, PDI protein disulfide isomerase, SFA saturated fatty acid, UFA unsaturated fatty acid, VLDL very low-density lipoprotein.