ArticleScientific reports2023
Hepcidin deficiency in mice impairs white adipose tissue browning possibly due to a defect in de novo adipogenesis.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Modulation of hepcidin synthesis: the core link in the bi-directional relationship between iron and obesity.Reviews in endocrine & metabolic disorders · 2026Review
- Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025Review
- Iron homeostasis and insulin sensitivity: unraveling the complex interactions.Reviews in endocrine & metabolic disorders · 2024Review
- A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue.Autophagy reports · 2024Article
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of iron in the two major sites of adaptive thermogenesis, namely the beige inguinal (iWAT) and brown adipose tissues (BAT) has not been fully understood yet. Body iron levels and distribution is controlled by the iron regulatory peptide hepcidin. Here, we explored iron homeostasis and thermogenic activity in brown and beige fat in wild-type and iron loaded Hepcidin KO mice. Hepcidin-deficient mice displayed iron overload in both iWAT and BAT, and preferential accumulation of ferritin in stromal cells compared to mature adipocytes. In contrast to BAT, the iWAT of Hepcidin KO animals featured with defective thermogenesis evidenced by an altered beige signature, including reduced UCP1 levels and decreased mitochondrial respiration. This thermogenic modification appeared cell autonomous and persisted after a 48 h-cold challenge, a potent trigger of thermogenesis, suggesting compromised de novo adipogenesis. Given that WAT browning occurs in both mice and humans, our results provide physiological results to interrogate the thermogenic capacity of patients with iron overload disorders.
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