ArticleNature metabolism2025
Haem biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue.
Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Folic acid polyglutamylation triggers MAP2K5 signaling to induce adipocyte lipid catabolism.bioRxiv : the preprint server for biology · 2026Article
- Brown fat protects against hepatic oxidative stress by remodeling the circulating metabolome.Cell metabolism · 2026Article
- Nitrate-Sialin2 axis couples ER-mitochondrial calcium signaling with fatty acid metabolism to drive white adipose browning.Nature communications · 2026Article
- Article
- Phytosterols improve feed efficiency in yaks by enriching rumen Succiniclasticum.Animal microbiome · 2026Article
- An extended network for regulation of heme homeostasis in cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Alteration of the follicular fluid amino acid profile reveals the important roles of several amino acids in embryo quality in patients with polycystic ovary syndrome.Reproductive biology and endocrinology : RB&E · 2025Article
- Creatine kinase B mediates UCP1-independent beige fat thermogenesis via the futile creatine cycle in mice.Molecular metabolism · 2025Article
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Abstract
The distinctive colour of brown adipose tissue (BAT) is attributed to its high content of haem-rich mitochondria. However, the mechanisms by which BAT regulates intracellular haem levels remain largely unexplored. Here we demonstrate that haem biosynthesis is the primary source of haem in brown adipocytes. Inhibiting haem biosynthesis results in an accumulation of the branched-chain amino acids (BCAAs) valine and isoleucine, owing to a haem-associated metabolon that channels BCAA-derived carbons into haem biosynthesis. Haem synthesis-deficient brown adipocytes display reduced mitochondrial respiration and lower UCP1 levels than wild-type cells. Although exogenous haem supplementation can restore intracellular haem levels and mitochondrial function, UCP1 downregulation persists. This sustained UCP1 suppression is linked to epigenetic regulation induced by the accumulation of propionyl-CoA, a byproduct of disrupted haem synthesis. Finally, disruption of haem biosynthesis in BAT impairs thermogenic response and, in female but not male mice, hinders the cold-induced clearance of circulating BCAAs in a sex-hormone-dependent manner. These findings establish adipose haem biosynthesis as a key regulator of thermogenesis and sex-dependent BCAA homeostasis.
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