ArticleJournal of lipid research2024
Disruption of nucleotide biosynthesis reprograms mitochondrial metabolism to inhibit adipogenesis.
Article in Journal of lipid research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dietary Nucleotides as Potential Modulators of Inflammatory and Metabolic Pathways with Implications for Insulin Resistance.International journal of molecular sciences · 2026Review
- Dynamic control of nucleotide metabolism in physiology and disease.Nature cell biology · 2026Review
- Gut Microbiota-Derived Metabolites to Regulate Intramuscular Fat Deposition in Pigs.Microorganisms · 2026Review
- Regulation of adipogenesis by nucleotides.Biochemical Society transactions · 2025Review
- Mitochondrial substrate oxidation regulates distinct cell differentiation outcomes.Trends in cell biology · 2025Article
- Systemic inhibition ofbioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
A key organismal response to overnutrition involves the development of new adipocytes through the process of adipogenesis. Preadipocytes sense changes in the systemic nutrient status and metabolites can directly modulate adipogenesis. We previously identified a role of de novo nucleotide biosynthesis in adipogenesis induction, whereby inhibition of nucleotide biosynthesis suppresses the expression of the transcriptional regulators PPARγ and C/EBPα. Here, we set out to identify the global transcriptomic changes associated with the inhibition of nucleotide biosynthesis. Through RNA sequencing (RNAseq), we discovered that mitochondrial signatures were the most altered in response to inhibition of nucleotide biosynthesis. Blocking nucleotide biosynthesis induced rounded mitochondrial morphology, and altered mitochondrial function, and metabolism, reducing levels of tricarboxylic acid cycle intermediates, and increasing fatty acid oxidation (FAO). The loss of mitochondrial function induced by suppression of nucleotide biosynthesis was rescued by exogenous expression of PPARγ. Moreover, inhibition of FAO restored PPARγ expression, mitochondrial protein expression, and adipogenesis in the presence of nucleotide biosynthesis inhibition, suggesting a regulatory role of nutrient oxidation in differentiation. Collectively, our studies shed light on the link between substrate oxidation and transcription in cell fate determination.
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Registered trials
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