ArticleInternational journal of obesity (2005)2025
Interleukin-33 promotes lipolysis of adipocytes and protects male mice against obesity via activation of β-adrenergic receptor signaling.
Article in International journal of obesity (2005), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Bridging exercise biology and immunometabolism: A novel irisin pathway toward next-generation metabolic and neurodegenerative therapies.Metabolism open · 2026Review
- Targeting Inflammation with Dietary ω-3 Polyunsaturated Fatty Acids Improved Lipid Mobilization and Flux in Heat-Stressed Wether Lambs.Metabolites · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
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7 authors.
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Abstract
backgroundTargeting intracellular lipolysis represents a therapeutic potential for treating metabolic disorders such as obesity. Interleukin (IL)-33 has been shown to exert anti-obesity effects by reducing inflammation and restricting adipocyte hypertrophy.
methodsIn this study, male mice on a high-fat diet (HFD) were treated with IL-33 once every 2 days for 2 weeks. 3T3-L1 cells were treated with IL-33 to verify the down-stream effect of β1-AR activation on the adipose cells.
resultsIL-33 treatment led to a reduction in adipose tissue mass and a decreased in lipid deposition in male mice with obesity, accompanied by activation of β-adrenergic receptor (β-AR) signals. Immunostaining for tyrosine hydroxylase (TH) revealed an increase of TH within the adipose tissue in male mice. Metabolomic analysis showed that IL-33 induced a distinct metabolic profile in differentiated adipocytes, with significant changes in metabolites related to lipolysis pathways. Supplementation with β1-AR inhibitor significantly inhibited IL-33-induced p-HSL and p-PKA activation. Compared to IL-33 alone, β1-AR inhibitor reduced glycerol release and increased accumulation of lipid droplets. We also illustrated the fatty acids (FAs) process by tracking FA trafficking, and found that the labeled FA localized lipid droplets (LDs) in mature adipocytes but shifted from LDs to mitochondria at 20 ng/mL IL-33.
conclusionWe summarized that IL-33 regulated mature adipocyte metabolism and enhanced lipolysis in male mice via activation of the β-AR/cAMP/PKA/HSL signaling pathway. However, given that sex is a significant determinant in obesity, future studies should investigate potential sex-specific effects of IL-33 in metabolic regulation.
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