ArticleNature communications2025
Differential transport pathways of saturated and unsaturated fatty acid esters in male mouse hepatocytes.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Stem Cell-Derived Exosomes Improve Neurological Dysfunction in a Rat Model of Moderate-to-Severe Cerebral Palsy.Stem cell reviews and reports · 2026Article
- Bta-miR-30f promotes adipogenesis and unsaturated fatty acid accumulation by targetingiScience · 2026Article
- Protein disulfide isomerase A6 (PDIA6) is essential for acrosome biogenesis and male fertility in mice.Cell communication and signaling : CCS · 2026Article
- Targeting the ER stress sensor IRE1 protects the liver from fibrosis through the downregulation of the proteostasis factor P4HB/PDIA1.Hepatology (Baltimore, Md.) · 2026Article
- Current and Emerging Issues in Familial Hypobetalipoproteinemia-related Steatotic Liver Diseases.Journal of clinical and translational hepatology · 2025Review
- The beneficial effect of hepatic ER stress-associated protein PDI on obesity-associated glucose dysregulation.Nutrition & metabolism · 2025Article
- Magnesium Promotes Growth-Metabolism Balance in Juvenile Largemouth Bass (Antioxidants (Basel, Switzerland) · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Saturated fatty acid (SFA) and unsaturated fatty acid (UFA) have distinct impacts on health. Whether SFA and UFA are differentially transported in liver remains elusive. Here, we find the secretion of UFA but not SFA esters is retarded in a male mouse hepatic endoplasmic reticulum (ER) stress model. Among 13 members of protein disulfide isomerase (PDI) family, only PDIA1 (PDI) deficiency leads to hepatosteatosis and hypolipidemia. In PDI-deficient male mouse liver, there is a severe accumulation but secretory blockade of UFA esters, whereas the accumulation and secretion of SFA esters remain normal. PDI catalyzes the oxidative folding of microsomal triglyceride transfer protein (MTP). In addition, PDI deficiency in hepatocytes abolishes Apolipoprotein B-100 (ApoB-100) very low-density lipoprotein (VLDL) secretion while maintaining partial ApoB-48 VLDL secretion. In summary, we find that the secretion of UFA esters is PDI-MTP indispensable, while SFA esters could be transferred out of liver via ApoB-48 VLDL through a PDI-MTP-independent pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.