Pyrimidines maintain mitochondrial pyruvate oxidation to support de novo lipogenesis

Umakant Sahu, Elodie Villa, Colleen R. Reczek, Zibo Zhao, Brendan P. O’Hara, Michael D. Torno, Rohan Mishra, William D. Shannon, John M. Asara, Peng Gao, Ali Shilatifard, Navdeep S. Chandel, Issam Ben-Sahra*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

Cellular purines, particularly adenosine 5′-triphosphate (ATP), fuel many metabolic reactions, but less is known about the direct effects of pyrimidines on cellular metabolism. We found that pyrimidines, but not purines, maintain pyruvate oxidation and the tricarboxylic citric acid (TCA) cycle by regulating pyruvate dehydrogenase (PDH) activity. PDH activity requires sufficient substrates and cofactors, including thiamine pyrophosphate (TPP). Depletion of cellular pyrimidines decreased TPP synthesis, a reaction carried out by TPP kinase 1 (TPK1), which reportedly uses ATP to phosphorylate thiamine (vitamin B1). We found that uridine 5′-triphosphate (UTP) acts as the preferred substrate for TPK1, enabling cellular TPP synthesis, PDH activity, TCA-cycle activity, lipogenesis, and adipocyte differentiation. Thus, UTP is required for vitamin B1 utilization to maintain pyruvate oxidation and lipogenesis.

Original languageEnglish (US)
Pages (from-to)1484-1492
Number of pages9
JournalScience
Volume383
Issue number6690
DOIs
StatePublished - Mar 29 2024

ASJC Scopus subject areas

  • General

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