ArticleThe Journal of biological chemistry2010
Genetic ablation of calcium-independent phospholipase A2gamma prevents obesity and insulin resistance during high fat feeding by mitochondrial uncoupling and increased adipocyte fatty acid oxidation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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.
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Who cites it
48 citing papers in PubMed, 90 citations in OpenAlex.
- Human cardiovascular disease IBC chip-wide association with weight loss and weight regain in the look AHEAD trial.Human heredity · 2013Trial
- Phospholipases: Where Do We Stand?Methods in molecular biology (Clifton, N.J.) · 2027Review
- The balancing act between lipid droplets and lysosomes for membrane functionality in age-related neurodegeneration and inflammation.Progress in lipid research · 2025Review
- Recent Progress inInternational journal of molecular sciences · 2025Review
- Genetic deletion of calcium-independent phospholipase A2γ protects mice from diabetic nephropathy.PloS one · 2024Article
- Beneficial Effects of Halogenated Anesthetics in Cardiomyocytes: The Role of Mitochondria.Antioxidants (Basel, Switzerland) · 2023Review
- Lipid remodeling of adipose tissue in metabolic health and disease.Experimental & molecular medicine · 2023Review
- Genetic deletion of skeletal muscle iPLAiScience · 2023Article
- Review
- Article
- Mitochondrial HAnnual review of physiology · 2022Review
- Ether Lipids in Obesity: From Cells to Population Studies.Frontiers in physiology · 2022Review
- LRG1 is an adipokine that mediates obesity-induced hepatosteatosis and insulin resistance.The Journal of clinical investigation · 2021Article
- Identification and expression of phospholipase A2 genes related to transcriptional control in the interleukin-17A/F1 pathway in the intestines of Japanese medakaFish and shellfish immunology reports · 2021Article
- Rescue of Hepatic Phospholipid Remodeling Defectin iPLA2β-Null Mice Attenuates Obese but Not Non-Obese Fatty Liver.Biomolecules · 2020Review
- 12-LOX catalyzes the oxidation of 2-arachidonoyl-lysolipids in platelets generating eicosanoid-lysolipids that are attenuated by iPLAThe Journal of biological chemistry · 2020Article
- Genetic Ablation of Calcium-independent Phospholipase AScientific reports · 2019Article
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Loss of mitochondrial protease ClpP protects mice from diet-induced obesity and insulin resistance.EMBO reports · 2018Article
- Enriching the Starter Diet in n-3 Polyunsaturated Fatty Acids Reduces Adipocyte Size in Broiler Chicks.Current developments in nutrition · 2017Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Phospholipases are critical enzyme mediators participating in many aspects of cellular function through modulating the generation of lipid 2nd messengers, membrane physical properties, and cellular bioenergetics. Here, we demonstrate that mice null for calcium-independent phospholipase A(2)γ (iPLA(2)γ(-/-)) are completely resistant to high fat diet-induced weight gain, adipocyte hypertrophy, hyperinsulinemia, and insulin resistance, which occur in iPLA(2)γ(+/+) mice after high fat feeding. Notably, iPLA(2)γ(-/-) mice were lean, demonstrated abdominal lipodystrophy, and remained insulin-sensitive despite having a marked impairment in glucose-stimulated insulin secretion after high fat feeding. Respirometry of adipocyte explants from iPLA(2)γ(-/-) mice identified increased rates of oxidation of multiple different substrates in comparison with adipocyte explants from wild-type littermates. Shotgun lipidomics of adipose tissue from wild-type mice demonstrated the anticipated 2-fold increase in triglyceride content after high fat feeding. In sharp contrast, the adipocyte triglyceride content was identical in iPLA(2)γ(-/-) mice fed either a standard diet or a high fat diet. Respirometry of skeletal muscle mitochondria from iPLA(2)γ(-/-) mice demonstrated marked decreases in state 3 respiration using multiple substrates whose metabolism was uncoupled from ATP production. Shotgun lipidomics of skeletal muscle revealed a decreased content of cardiolipin with an altered molecular species composition thereby identifying the mechanism underlying mitochondrial uncoupling in the iPLA(2)γ(-/-) mouse. Collectively, these results identify iPLA(2)γ as an obligatory upstream enzyme that is necessary for efficient electron transport chain coupling and energy production through its participation in the alterations of cellular bioenergetics that promote the development of the metabolic syndrome.
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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.