ArticleJournal of lipid research2012
Characterization of an arachidonic acid-deficient (Fads1 knockout) mouse model.
Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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.
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Who cites it
50 citing papers in PubMed, 76 citations in OpenAlex.
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- Dynamic allelic expression in mouse mammary glands across the adult developmental cycle.Nucleic acids research · 2025Article
- Arachidonic acid in aging: New roles for old players.Journal of advanced research · 2025Review
- Omega-3 Fatty Acids and Chronic Lung Diseases: A Narrative Review of Impacts from Womb to Tomb.The Journal of nutrition · 2025Review
- Hepatocyte-SpecificInternational journal of molecular sciences · 2024Article
- GWAS-identified bipolar disorder risk allele in the FADS1/2 gene region links mood episodes and unsaturated fatty acid metabolism in mutant mice.Molecular psychiatry · 2023Article
- Lipid droplets and polyunsaturated fatty acid trafficking: Balancing life and death.Frontiers in cell and developmental biology · 2023Review
- Associations of fatty acids composition and estimated desaturase activities in erythrocyte phospholipids with biochemical and clinical indicators of cardiometabolic risk in non-diabetic Serbian women: the role of level of adiposity.Frontiers in nutrition · 2023Article
- Omega-6 highly unsaturated fatty acids in Leydig cells facilitate male sex hormone production.Communications biology · 2022Article
- Chromatin conformation of human oral epithelium can identify orofacial cleft missing functional variants.International journal of oral science · 2022Article
- Disruption of the circadian clock component BMAL1 elicits an endocrine adaption impacting on insulin sensitivity and liver disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A mouse model of gestational diabetes shows dysregulated lipid metabolism post-weaning, after return to euglycaemia.Nutrition & diabetes · 2022Article
- Review
- Embryonic fatty acid metabolism in diabetic pregnancy: the difference between embryoblasts and trophoblasts.Molecular human reproduction · 2020Article
- Roles of polyunsaturated fatty acids, from mediators to membranes.Journal of lipid research · 2020Review
- Effects of high-fat diet and intestinal aryl hydrocarbon receptor deletion on colon carcinogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression.iScience · 2020Article
- Lipid Related Genes Altered in NASH Connect Inflammation in Liver Pathogenesis Progression to HCC: A Canonical Pathway.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arachidonic acid (20:4(Δ5,8,11,14), AA)-derived eicosanoids regulate inflammation and promote cancer development. Previous studies have targeted prostaglandin enzymes in an attempt to modulate AA metabolism. However, due to safety concerns surrounding the use of pharmaceutical agents designed to target Ptgs2 (cyclooxygenase 2) and its downstream targets, it is important to identify new targets upstream of Ptgs2. Therefore, we determined the utility of antagonizing tissue AA levels as a novel approach to suppressing AA-derived eicosanoids. Systemic disruption of the Fads1 (Δ5 desaturase) gene reciprocally altered the levels of dihomo-γ-linolenic acid (20:3(Δ8,11,14), DGLA) and AA in mouse tissues, resulting in a profound increase in 1-series-derived and a concurrent decrease in 2-series-derived prostaglandins. The lack of AA-derived eicosanoids, e.g., PGE₂ was associated with perturbed intestinal crypt proliferation, immune cell homeostasis, and a heightened sensitivity to acute inflammatory challenge. In addition, null mice failed to thrive, dying off by 12 weeks of age. Dietary supplementation with AA extended the longevity of null mice to levels comparable to wild-type mice. We propose that this new mouse model will expand our understanding of how AA and its metabolites mediate inflammation and promote malignant transformation, with the eventual goal of identifying new drug targets upstream of Ptgs2.
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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 OpenQuestion graph.