Loss of peroxisomal membrane proteins PEX13 and PEX14 in liver cells altered lipid metabolism gene expression, promoting increased fatty acid uptake and synthesis.
Peroxisomal dysfunction via PEX13 and PEX14 knockdown disrupts hepatic metabolic pathways, promoting increased fatty acid uptake and synthesis in a liver cell line model.
Absolute Event Rate: 0% vs 0%
Peroxisomal disorders arise from severe peroxisome dysfunction and are frequently linked to liver pathology. Metabolic dysfunction-associated steatotic liver disease, which affects up to 38% of adults worldwide, has driven extensive efforts to identify genes that contribute to its development. In this study, we investigated the role of two peroxisomal membrane proteins, PEX13 and PEX14, by performing single and dual siRNA‑mediated knockdowns in a liver cell line, HUH‑7. Steatosis was induced using free fatty acids, and changes in lipid‑metabolism gene expression were assessed by qRT‑PCR. Knockdown efficiency reached 90% for both genes, and Oil-Red-O staining confirmed successful induction of steatosis. Both single and combined knockdown of PEX13 and PEX14 altered the expression of genes involved in lipid sensing, fatty acid uptake, synthesis, and oxidation. These findings suggest that peroxisomal dysfunction disrupts hepatic metabolic pathways, promoting increased fatty acid uptake and synthesis. Such alterations may contribute to the liver dysfunction observed in patients with peroxisome biogenesis disorders, highlighting the importance of peroxisomal integrity in maintaining lipid homeostasis.
Vinoy et al. (Fri,) reported a other. Loss of peroxisomal membrane proteins PEX13 and PEX14 in liver cells altered lipid metabolism gene expression, promoting increased fatty acid uptake and synthesis.