ArticleLipids2009
Hepatic expression of long-chain acyl-CoA synthetase 3 is upregulated in hyperlipidemic hamsters.
Article in Lipids, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The Diagnostic Value of ACSL1, ACSL4, and ACSL5 and the Clinical Potential of an ACSL Inhibitor in Non-Small-Cell Lung Cancer.Cancers · 2024Article
- ACSL4 as a Potential Target and Biomarker for Anticancer: From Molecular Mechanisms to Clinical Therapeutics.Frontiers in pharmacology · 2022Review
- Immunohistochemical staining reveals differential expression of ACSL3 and ACSL4 in hepatocellular carcinoma and hepatic gastrointestinal metastases.Bioscience reports · 2020Article
- Liver-specific knockdown of long-chain acyl-CoA synthetase 4 reveals its key role in VLDL-TG metabolism and phospholipid synthesis in mice fed a high-fat diet.American journal of physiology. Endocrinology and metabolism · 2019Article
- Exogenous Monounsaturated Fatty Acids Promote a Ferroptosis-Resistant Cell State.Cell chemical biology · 2019Article
- PPARδ activation induces hepatic long-chain acyl-CoA synthetase 4 expression in vivo and in vitro.Biochimica et biophysica acta · 2015Article
- Modeling human Coenzyme A synthase mutation in yeast reveals altered mitochondrial function, lipid content and iron metabolism.Microbial cell (Graz, Austria) · 2015Article
- Long-chain acyl-CoA synthetase in fatty acid metabolism involved in liver and other diseases: an update.World journal of gastroenterology · 2015Review
- Arachidonic acid downregulates acyl-CoA synthetase 4 expression by promoting its ubiquitination and proteasomal degradation.Journal of lipid research · 2014Article
- Acyl-CoA metabolism and partitioning.Annual review of nutrition · 2014Review
- Molecular cloning of the goose ACSL3 and ACSL5 coding domain sequences and their expression characteristics during goose fatty liver development.Molecular biology reports · 2014Article
- Influence of fish oil on skeletal muscle mitochondrial energetics and lipid metabolites during high-fat diet.American journal of physiology. Endocrinology and metabolism · 2013Article
- High-fructose diet downregulates long-chain acyl-CoA synthetase 3 expression in liver of hamsters via impairing LXR/RXR signaling pathway.Journal of lipid research · 2013Article
- Delineation of molecular pathways that regulate hepatic PCSK9 and LDL receptor expression during fasting in normolipidemic hamsters.Atherosclerosis · 2012Article
- Long chain acyl-CoA synthetase-3 is a molecular target for peroxisome proliferator-activated receptor delta in HepG2 hepatoma cells.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Members of the mammalian long-chain acyl-CoA synthetase (ACSL) family are key enzymes for cellular fatty acid metabolism that catalyze the initial step in activation of long-chain fatty acids. However, the specificity of individual isoforms of ACSL to the lipid metabolic process is not well studied. In addition, the regulation of expression of individual ACSL isoforms under hyperlipidemic conditions is largely unknown. We cloned the hamster ACSL3 cDNA coding region and generated specific antibodies recognizing the ACSL3 protein. We next observed the changes in ACSL3 mRNA and protein expression in hamsters fed a standard chow diet or a high fat and high cholesterol (HFHC) diet. HFHC feeding significantly increased ACSL3 mRNA and protein expression in liver and to a lesser extent in muscle but not in adipose, brain, heart, or testis. Additionally, ACSL3 mRNA abundance was differentially regulated by the nutritional status in different tissues with liver, muscle, and adipose being the most sensitive tissues. Importantly, the hepatic ACSL3 mRNA expression pattern in response to fasting and refeeding in hyperlipidemic hamsters differed from that observed in normal chow-fed hamsters. Together, these results provide the first in vivo evidence of altered regulation of hepatic ACSL3 expression under hyperlipidemic conditions and suggest important regulatory roles for this enzyme in lipid metabolism.
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What OpenQuestion holds
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 OpenQuestion graph.