ArticleJournal of lipid research2013
Fas activates lipolysis in a Ca2+-CaMKII-dependent manner in 3T3-L1 adipocytes.
Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
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- CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Calcium/Calmodulin-Dependent Protein Kinase II Inhibitors Mitigate High-Fat Diet-Induced Obesity in Mice.Journal of obesity · 2025Article
- Synergistic Effect ofBiology · 2024Article
- Cytosolic calcium regulates hepatic mitochondrial oxidation, intrahepatic lipolysis, and gluconeogenesis via CAMKII activation.Cell metabolism · 2024Article
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- Anti-adipogenic effect ofFood science and biotechnology · 2020Article
- Impact of Conventional and Atypical MAPKs on the Development of Metabolic Diseases.Biomolecules · 2020Review
- Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication.Journal of lipid research · 2019Review
- Peptide/Receptor Co-evolution Explains the Lipolytic Function of the Neuropeptide TLQP-21.Cell reports · 2019Article
- Adipocyte dysfunction, inflammation and metabolic syndrome.Reviews in endocrine & metabolic disorders · 2014Review
- Systematic lipidomic analysis of yeast protein kinase and phosphatase mutants reveals novel insights into regulation of lipid homeostasis.Molecular biology of the cell · 2014Article
- Efficient in vitro adipocyte model of long-term lipolysis: a tool to study the behavior of lipophilic compounds.In vitro cellular & developmental biology. Animal · 2014Article
- Article
- Trichostatin A modulates thiazolidinedione-mediated suppression of tumor necrosis factor α-induced lipolysis in 3T3-L1 adipocytes.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fas (CD95) is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a crucial role in the induction of apoptosis. However, like TNF, Fas can induce nonapoptotic signaling pathways. We previously demonstrated that mice lacking Fas specifically in adipocytes are partly protected from diet-induced insulin resistance, potentially via decreased delivery of FAs to the liver, as manifested by lower total liver ceramide content. In the present study, we aimed to delineate the signaling pathway involved in Fas-mediated adipocyte lipid mobilization. Treatment of differentiated 3T3-L1 adipocytes with membrane-bound Fas ligand (FasL) significantly increased lipolysis after 12 h without inducing apoptosis. In parallel, Fas activation increased phosphorylation of ERK1/2, and FasL-induced lipolysis was blunted in the presence of the ERK-inhibitor U0126 or in ERK1/2-depleted adipocytes. Furthermore, Fas activation increased phosphorylation of the Ca(2+)/calmodulin-dependent protein kinases II (CaMKII), and blocking of the CaMKII-pathway (either by the Ca(2+) chelator BAPTA or by the CaMKII inhibitor KN62) blunted FasL-induced ERK1/2 phosphorylation and glycerol release. In conclusion, we propose a novel role for CaMKII in promoting lipolysis in adipocytes.
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