ArticleExperimental and molecular pathology2007
Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice.
Article in Experimental and molecular pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- GPAM mediates mitochondrial dysfunction and the progression of alcoholic liver disease through lipid remodeling.Science advances · 2026Article
- GPAM upregulation enhances hepatic fat deposition and reduces visceral adipose tissue in response to trans-fatty acids.Journal of gastroenterology · 2025Article
- Lipid biosynthesis enzyme Agpat5 in AgRP-neurons is required for insulin-induced hypoglycemia sensing and glucagon secretion.Nature communications · 2022Article
- Puerarin ameliorates nonalcoholic fatty liver in rats by regulating hepatic lipid accumulation, oxidative stress, and inflammation.Frontiers in immunology · 2022Article
- Hepatic lipid droplets: A balancing act between energy storage and metabolic dysfunction in NAFLD.Molecular metabolism · 2021Review
- Intramuscular triglyceride synthesis: importance in muscle lipid partitioning in humans.American journal of physiology. Endocrinology and metabolism · 2018Article
- How lipid droplets "TAG" along: Glycerolipid synthetic enzymes and lipid storage.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Glycerol-3-phosphate acyltransferase-1 upregulation by O-GlcNAcylation of Sp1 protects against hypoxia-induced mouse embryonic stem cell apoptosis via mTOR activation.Cell death & disease · 2016Article
- Article
- Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential for murine CD4(+) T cell metabolic activation.Biochimica et biophysica acta · 2014Article
- Chemical modulation of glycerolipid signaling and metabolic pathways.Biochimica et biophysica acta · 2014Review
- Glycerol-3-phosphate acyltransferase (GPAT)-1, but not GPAT4, incorporates newly synthesized fatty acids into triacylglycerol and diminishes fatty acid oxidation.The Journal of biological chemistry · 2013Article
- Mitochondria-type GPAT is required for mitochondrial fusion.The EMBO journal · 2013Article
- Mice deficient in glycerol-3-phosphate acyltransferase-1 have a reduced susceptibility to liver cancer.Toxicologic pathology · 2012Article
- Mammalian triacylglycerol metabolism: synthesis, lipolysis, and signaling.Chemical reviews · 2011Review
- Pharmacological glycerol-3-phosphate acyltransferase inhibition decreases food intake and adiposity and increases insulin sensitivity in diet-induced obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Early hepatic insulin resistance in mice: a metabolomics analysis.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Biochemistry, physiology, and genetics of GPAT, AGPAT, and lipin enzymes in triglyceride synthesis.American journal of physiology. Endocrinology and metabolism · 2009Review
- Glycerol-3-phosphate acyltransferase 1 is essential for the immune response to infection with coxsackievirus B3 in mice.The Journal of nutrition · 2009Article
- Regulation of Triglyceride Metabolism. II. Function of mitochondrial GPAT1 in the regulation of triacylglycerol biosynthesis and insulin action.American journal of physiology. Gastrointestinal and liver physiology · 2007Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The absence of mouse mitochondrial glycerol-3-phosphate acyltransferase-1 (Gpat1-/-) increases the amount of arachidonate in liver phospholipids and increases beta-hydroxybutyrate and acyl-carnitines, suggesting an elevated rate of liver fatty acid oxidation. We asked whether these alterations might increase reactive oxygen species (ROS), apoptosis, or hepatocyte proliferation. Compared to wildtype controls, liver mitochondria from Gpat1-/- mice showed a 20% increase in the rate of ROS production and a markedly increased sensitivity to the induction of the mitochondrial permeability transition. Mitochondrial phosphatidylethanolamine and phosphatidylcholine from Gpat1-/- liver contained 21% and 67% more arachidonate, respectively, than wildtype controls, and higher amounts of 4-hydroxynonenal, a product of arachidonate peroxidation. Oxidative stress was associated with an increase in apoptosis, and with 3-fold and 15-fold higher TUNEL positive cells in liver from young and old Gpat1-/- mice, respectively, compared to age-matched controls. Compared to controls, bromodeoxyuridine labeling was 50% and 7-fold higher in livers from young and old Gpat1-/- mice, respectively, but fewer glutathione-S-transferase positive cells were present. Thus, Gpat1-/- liver exhibits increased oxidative stress and sensitivity of the mitochondrial permeability transition pore, and a balanced increase in apoptosis and proliferation.
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