ArticleJournal of cancer prevention2013
Global Inactivation of the Pla2g6 Gene in Mice Does Not Cause Dyslipidemia under Chow or High-fat Diet Conditions.
Article in Journal of cancer prevention, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Distinct Roles of Myeloid- and Hepatocyte-PLA2G6 Deletion in Mice With Metabolic Dysfunction-Associated Steatotic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Genome-wide discovery of genetic loci that uncouple excess adiposity from its comorbidities.Nature metabolism · 2021Article
- Rescue of Hepatic Phospholipid Remodeling Defectin iPLA2β-Null Mice Attenuates Obese but Not Non-Obese Fatty Liver.Biomolecules · 2020Review
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Candidate Regulators of Dyslipidemia in Chromosome 1 Substitution Lines Using Liver Co-Expression Profiling Analysis.Frontiers in genetics · 2019Article
- Calcium-independent phospholipases A2 and their roles in biological processes and diseases.Journal of lipid research · 2015Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenome-wide association studies suggest that plasma triacylglyceride (TAG) in humans was associated with variation in the PLA2G6 locus, a gene that encodes calcium-independent phospholipase A2 (iPLA2 β). The objective of the present study is to understand the impact of genetic inactivation of iPLA2 β on hepatic TAG metabolism in C57BL/6 mice.
methodsMale iPLA2 β (+) (/-) mice were backcrossed with female iPLA2 β (-/-) mice for up to 10 generations prior to experiments. Lipid and lipoprotein metabolism from plasma, hepatocytes, thigh subcutaneous adipose and thigh skeletal muscle tissues of the mice were determined under various experimental conditions.
resultsThe iPLA2 β (-/-) mice, either male or female as compared with iPLA2 β (+) (/) (+) littermates, showed no change in fasted or postprandial plasma TAG or total cholesterol at young (12-15 weeks) or old (40-44 weeks) ages under chow diet or high-fat diet (HFD) conditions. However, fractionation of plasma lipoproteins showed that under HFD conditions, there was a significant increase (by 40%) in apoB-100 association with VLDL1 fractions in iPLA2 β (-/-) mice as compared with iPLA2 β (+) (/) (+) littermates. There was no significant difference in triglyceride or cholesterol contents in the liver, muscle, or adipose tissue between iPLA2 β (-/-) and iPLA2 β (+/+) littermates. Metabolic labeling experiments with cultured primary hepatocytes isolated from iPLA2 β (-/-) mice also showed 2-fold increase in the secretion of [(35)S]methionine-labeled apoB-100 in VLDL1 fractions as compared with that from iPLA2 β (+) (/) (+) hepatocytes. Likewise, secretion of [(3)H]palmitate-labeled TAG from the iPLA2 β (-/-) hepatocytes was increased by 2-fold.
conclusionsAlthough iPLA2 β may play a role in TAG-rich VLDL1 production from cultured hepatocytes, there is no evidence that inactivation of iPLA2 β would lead to dyslipidemia in mice in vivo.
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