ArticleThe Journal of biological chemistry2011
Relative contribution of adipose triglyceride lipase and hormone-sensitive lipase to tumor necrosis factor-α (TNF-α)-induced lipolysis in adipocytes.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 107 citations in OpenAlex.
- α-Linolenic acid increases the G0/G1 switch gene 2 mRNA expression in peripheral blood mononuclear cells from obese patients: a pilot study.Lipids in health and disease · 2016Trial
- Pro-inflammatory cytokine-driven molecular signaling in skeletal muscle during cancer cachexia.Biochemical Society transactions · 2026Review
- Novel Insights into G0S2 as a Central Regulator of Lipid Metabolism and Its Implications for Meat Quality.Animals : an open access journal from MDPI · 2026Review
- The Eubacterium Rectale Derived Extracellular Vesicles Alleviate Cancer Cachexia Induced Lipolysis by Inhibiting Macrophage Polarization.Journal of extracellular vesicles · 2026Article
- Fatty Acids and Their Roles in Cardiac Physiology and Pathology: Mechanistic and Interventional Studies.Nutrients · 2026Review
- Article
- TNF/TNFR1 is a Key Regulator of Prolonged Fasting-Induced Decrease in Adipose Tissue.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Risk factors for drug-related cachexia: an analysis based on the FDA adverse event reporting system (FAERS) from 2004 to 2025.Frontiers in pharmacology · 2026Article
- The triglyceride-glucose index in chronic kidney disease: a narrative review.Frontiers in nutrition · 2026Review
- DNA methylation reshapes the expression of adipokines and adipose factors in white adipose tissues.Epigenetics & chromatin · 2025Review
- Recent advances on the role of G0S2.Discover oncology · 2025Review
- MUSTN1 and FABP3 interact to regulate adipogenesis and lipid deposition.Journal of lipid research · 2025Article
- From fat storage to immune hubs: the emerging role of adipocytes in coordinating the immune response to infection.The FEBS journal · 2025Review
- Role of transforming growth factor-β1 in regulating adipocyte progenitors.Scientific reports · 2025Article
- G-protein-coupled receptor 84 regulates acute inflammation in normal and diabetic skin wounds.Cell reports · 2024Article
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- Article
- TNFα Effects on Adipocytes Are Influenced by the Presence of Lysine Methyltransferases, G9a (EHMT2) and GLP (EHMT1).Biology · 2023Article
- Recent advances in the crosstalk between adipose, muscle and bone tissues in fish.Frontiers in endocrinology · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
TNF-α potently stimulates basal lipolysis in adipocytes, which may contribute to hyperlipidemia and peripheral insulin resistance in obesity. Recent studies show that adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) act sequentially in catalyzing the first two steps of adipose lipolysis in response to β-adrenergic stimulation. Here, we sought to determine their functional roles in TNF-α-induced lipolysis. Silencing of ATGL expression in adipocytes almost completely abolished basal and TNF-α-induced glycerol release. In comparison, the glycerol release under the same conditions was only partially decreased upon reduction in expression of either HSL or the ATGL coactivator CGI-58. Interestingly, overexpression of ATGL restored the lipolytic rates in cells with silenced HSL or CGI-58, indicating a predominant role for ATGL. While expression of ATGL, HSL and CGI-58 remains mostly unaffected, TNF-α treatment caused a rapid abrogation of the ATGL inhibitory protein G0S2. TNF-α drastically decreased the level of G0S2 mRNA, and the level of G0S2 protein could be maintained by inhibiting proteasomal protein degradation using MG-132. Furthermore, coexpression of G0S2 was able to significantly decrease TNF-α-stimulated lipolysis mediated by overexpressed ATGL or CGI-58. We propose that the early reduction in G0S2 content is permissive for TNF-α-induced lipolysis.
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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.