ArticleNature communications2022
IL-1R-IRAKM-Slc25a1 signaling axis reprograms lipogenesis in adipocytes to promote diet-induced obesity in mice.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 21 citations in OpenAlex.
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- PRMT3-mediated post-translational adaptation to fasting regulates metabolic flexibility.Nature communications · 2026Article
- Mitochondrial arginase 2 regulates hematopoietic and cardiovascular adaptation to hypoxia.Blood vessels, thrombosis & hemostasis · 2026Article
- Relationship Between BMI and Prediabetes in Chinese Adults: A Cross-Sectional Analytical Study.International journal of endocrinology · 2025Article
- IL-1β promotes adipogenesis by directly targeting adipocyte precursors.Nature communications · 2024Article
- Association between protein-to-energy ratio and overweight/obesity in children and adolescents in the United States: a cross-sectional study based on NHANES.Frontiers in pediatrics · 2024Article
- Piperine alleviates nonalcoholic steatohepatitis by inhibiting NF-κB-mediated hepatocyte pyroptosis.PloS one · 2024Article
- Double-edged effect of sodium citrate in Nile tilapia (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Mutations in the Vicinity of the IRAK3 Guanylate Cyclase Center Impact Its Subcellular Localization and Ability to Modulate Inflammatory Signaling in Immortalized Cell Lines.International journal of molecular sciences · 2023Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Toll-like receptors/Interleukin-1 receptor signaling plays an important role in high-fat diet-induced adipose tissue dysfunction contributing to obesity-associated metabolic syndromes. Here, we show an unconventional IL-1R-IRAKM-Slc25a1 signaling axis in adipocytes that reprograms lipogenesis to promote diet-induced obesity. Adipocyte-specific deficiency of IRAKM reduces high-fat diet-induced body weight gain, increases whole body energy expenditure and improves insulin resistance, associated with decreased lipid accumulation and adipocyte cell sizes. IL-1β stimulation induces the translocation of IRAKM Myddosome to mitochondria to promote de novo lipogenesis in adipocytes. Mechanistically, IRAKM interacts with and phosphorylates mitochondrial citrate carrier Slc25a1 to promote IL-1β-induced mitochondrial citrate transport to cytosol and de novo lipogenesis. Moreover, IRAKM-Slc25a1 axis mediates IL-1β induced Pgc1a acetylation to regulate thermogenic gene expression in adipocytes. IRAKM kinase-inactivation also attenuates high-fat diet-induced obesity. Taken together, our study suggests that the IL-1R-IRAKM-Slc25a1 signaling axis tightly links inflammation and adipocyte metabolism, indicating a potential therapeutic target for obesity.
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