ArticleCell reports2025
Cold-inducible GOT1 activates the malate-aspartate shuttle in brown adipose tissue to support fuel preference for fatty acids.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- TRPA1 deficiency alters brown adipose tissue proteome and thermogenic gene expression during cold exposure in mice.Biochemistry and biophysics reports · 2026Article
- Fast & fuelious: the malate-aspartate shuttle in brown adipocyte lipid metabolism.The FEBS journal · 2026Article
- The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes.The FEBS journal · 2026Article
- Phosphomannomutase 1 restrains adipose thermogenic programming via inosine signaling.Molecular metabolism · 2026Article
- Cold exposure and metabolic health: Therapeutic potential for obesity, diabetes, and beyond.Physiological reports · 2026Review
- Repeated Cold Water Stress Leads to Improvements in Mitochondrial Metabolism of Skeletal Muscles in Rats.Metabolites · 2026Article
- Metabolomics Provides New Insights into the Mechanisms ofMicroorganisms · 2025Article
- The β-adrenergic receptor-SGK1 signaling pathway in brown adipocytes protects GOT1 from proteasomal degradation.Frontiers in cell and developmental biology · 2025Article
- Editorial: Deciphering signaling pathway interactions in tissue homeostasis.Frontiers in cell and developmental biology · 2025Article
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Abstract
Brown adipose tissue (BAT) simultaneously metabolizes fatty acids (FAs) and glucose under cold stress but favors FAs as the primary fuel for heat production. It remains unclear how BAT steers fuel preference toward FAs over glucose. Here, we show that the malate-aspartate shuttle (MAS) is activated by cold in BAT and plays a crucial role in promoting mitochondrial FA utilization. Mechanistically, cold stress selectively induces glutamic-oxaloacetic transaminase (GOT1), a key MAS enzyme, via the β-adrenergic receptor-PKA-PGC-1α axis. The increase in GOT1 activates MAS, transferring reducing equivalents from the cytosol to mitochondria. This process enhances FA oxidation in mitochondria while limiting glucose oxidation. In contrast, loss of MAS activity by GOT1 deficiency reduces FA oxidation, leading to increased glucose oxidation. Together, our work uncovers a unique regulatory mechanism and role for MAS in mitochondrial fuel selection and advances our understanding of how BAT maintains fuel preference for FAs under cold conditions.
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