Publication Date
2023
Journal or Book Title
Scientific Reports
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.
DOI
https://doi.org/10.1038/s41598-023-39305-0
Volume
13
License
UMass Amherst Open Access Policy
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Recommended Citation
Deschemin, Jean-Christiophe; Ransy, Céline; Bouillaud, Frédéric; Chung, Soonkyu; Galy, Bruno; Peyssonnaux, Carole; and Vaulont, Sophie, "Hepcidin deficiency in mice impairs white adipose tissue browning possibly due to a defect in de novo adipogenesis" (2023). Scientific Reports. 240.
https://doi.org/10.1038/s41598-023-39305-0