ArticleLipids2011
ApoB siRNA-induced liver steatosis is resistant to clearance by the loss of fatty acid transport protein 5 (Fatp5).
Article in Lipids, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- The bile acid-CoA ligase, FATP5, is necessary for the synthesis of N-acyl taurines in the liver.Journal of lipid research · 2026Article
- The Role of Phthalocyanine-Gold Nanoconjugates (Pc-Au NCs) in Ameliorating the Hepatic and Renal Toxicity-Induced by Silver Nanoparticles (Ag NPs) in Male Rats.Biological trace element research · 2024Article
- A computational framework to in silico screen for drug-induced hepatocellular toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- In vivo PAR-CLIP (viP-CLIP) of liver TIAL1 unveils targets regulating cholesterol synthesis and secretion.Nature communications · 2023Article
- LZP is required for hepatic triacylglycerol transportation through maintaining apolipoprotein B stability.PLoS genetics · 2021Article
- Monounsaturated Fatty Acids in Obesity-Related Inflammation.International journal of molecular sciences · 2020Review
- LC-N2G: a local consistency approach for nutrigenomics data analysis.BMC bioinformatics · 2020Article
- Bile acids mediated potential functional interaction between FXR and FATP5 in the regulation of Lipid Metabolism.International journal of biological sciences · 2020Review
- In Utero Dexamethasone Exposure Exacerbates Hepatic Steatosis in Rats That Consume Fructose During Adulthood.Nutrients · 2019Article
- Circadian clock component PERIOD2 regulates diurnal expression of NaScientific reports · 2018Article
- Fatty Acid Transport Proteins: Targeting FATP2 as a Gatekeeper Involved in the Transport of Exogenous Fatty Acids.MedChemComm · 2016Article
- Development of lipoprotein(a) siRNAs for mechanism of action studies in non-human primate models of atherosclerosis.Journal of cardiovascular translational research · 2015Article
- Rescue of Mtp siRNA-induced hepatic steatosis by DGAT2 siRNA silencing.Journal of lipid research · 2012Article
- mRNA knockdown by single strand RNA is improved by chemical modifications.Nucleic acids research · 2012Article
- SLC27 fatty acid transport proteins.Molecular aspects of medicineReview
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The association between hypercholesterolemia and elevated serum apolipoprotein B (APOB) has generated interest in APOB as a therapeutic target for patients at risk of developing cardiovascular disease. In the clinic, mipomersen, an antisense oligonucleotide (ASO) APOB inhibitor, was associated with a trend toward increased hepatic triglycerides, and liver steatosis remains a concern. We found that siRNA-mediated knockdown of ApoB led to elevated hepatic triglycerides and liver steatosis in mice engineered to exhibit a human-like lipid profile. Many genes required for fatty acid synthesis were reduced, suggesting that the observed elevation in hepatic triglycerides is maintained by the cell through fatty acid uptake as opposed to fatty acid synthesis. Fatty acid transport protein 5 (Fatp5/Slc27a5) is required for long chain fatty acid (LCFA) uptake and bile acid reconjugation by the liver. Fatp5 knockout mice exhibited lower levels of hepatic triglycerides due to decreased fatty acid uptake, and shRNA-mediated knockdown of Fatp5 protected mice from diet-induced liver steatosis. Here, we evaluated if siRNA-mediated knockdown of Fatp5 was sufficient to alleviate ApoB knockdown-induced steatosis. We determined that, although Fatp5 siRNA treatment was sufficient to increase the proportion of unconjugated bile acids 100-fold, consistent with FATP5's role in bile acid reconjugation, Fatp5 knockdown failed to influence the degree, zonal distribution, or composition of the hepatic triglycerides that accumulated following ApoB siRNA treatment.
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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 OpenQuestion graph.