ArticleBiomolecules2022
The Fibrinogen-like Domain of ANGPTL3 Facilitates Lipolysis in 3T3-L1 Cells by Activating the Intracellular Erk Pathway.
Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting ANGPTL3 and IL-33/ST2 Ameliorates Diabetic Kidney Disease by Reducing Lipotoxicity, Alleviating Inflammation and Inhibiting Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms and therapeutic potential of AMPK signaling pathway in the regulation of lipid metabolism.Molecular biology reports · 2026Review
- Urinary ANGPTL3: a novel noninvasive biomarker for podocyte injury in pediatric glomerular diseases.Journal of translational medicine · 2026Article
- ANGPTL3 as a target for treating lipid disorders in type 2 diabetes patients.Lipids in health and disease · 2024Review
- ANGPTL3 Deficiency and Risk of Hepatic Steatosis.Circulation · 2023Article
- Differential effects of bariatric surgery on plasma levels of ANGPTL3 and ANGPTL4.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2022Article
- Emerging Circulating Biomarkers in Atherosclerosis: From Molecular Mechanisms to Therapeutic Strategies.Biomolecules · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundANGPTL3 stimulates lipolysis in adipocytes, but the underlying molecular mechanism is yet unknown. The C-terminal fibrinogen-like domain of ANGPTL3 (ANGPTL3-Fld) activates the AKT pathway in endothelial cells. Hence, we evaluated whether ANGPTL3-Fld stimulates lipolysis in adipocytes through the MAPK kinase pathway. MATERIALS AND
methods3T3-L1 adipocytes were treated with isoproterenol (ISO), ANGPTL3-Fld, or both. Lipolysis was evaluated through the release of free fatty acids (FFAs) in the culture medium. The activation status of intracellular kinases was evaluated with and without the inhibition of the BRAF-ERK arm of the MAPK pathway.
resultsANGPTL3-Fld alone was not able to activate lipolysis, while the combination of ANGPTL3-Fld and ISO determined a 10-fold enrichment of the FFA concentration in the culture medium with an incremental effect (twofold) when compared with ISO alone. ANGPTL3-Fld alone inhibited hormone-sensitive lipase (HSL), whereas the treatment with ISO induced the activation of HSL. The net balance of ANGPTL3-Fld and ISO cotreatment resulted in HSL activation. The results indicate that ANGPTL3-Fld generated an intracellular activation signal involving the MAPK-ERK pathway, possibly through the PDGFRβ-PLCγ-AMPK axis.
conclusionANGPTL3-Fld appears to act as a facilitator of lipolysis in adipocytes, and this effect was driven by a signal mediated by a pathway that is different from the canonical β-adrenergic stimulus.
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