ArticleNature communications2026
PRMT3-mediated post-translational adaptation to fasting regulates metabolic flexibility.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Protein arginine methyltransferases as metabolic regulators: many roles beyond cancer.Science China. Life sciences · 2026Review
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Authors and funding
19 authors.
Funding
Abstract
Obesity impairs metabolic flexibility-the capacity to adapt to fluctuating energy demands. Emerging evidence suggests that dietary interventions, particularly time-restricted feeding (TRF), may help restore this flexibility. In this study, we demonstrate that feeding upregulates PRMT3 and asymmetric dimethylarginine (ADMA)-containing proteins via insulin-pAKT signaling, while fasting reduces their expression. Pharmacological inhibition of PRMT3 attenuates diet-induced obesity (DIO) and enhances adipocyte glycolysis in male mice. Mechanistically, PRMT3 drives the expression of citrate transporter SLC25A1 during feeding through direct arginine methylation. A 16:8 TRF regimen normalizes PRMT3 and ADMA levels while suppressing SLC25A1 expression. Notably, PRMT3 inhibition recapitulates the metabolic benefits of 16:8 TRF and improves metabolic flexibility. Furthermore, adipocyte-specific deletion of Slc25a1 in male mice protects against DIO and enhances insulin sensitivity. Collectively, these findings identify PRMT3-mediated arginine methylation in vWAT as a nutrient-responsive regulatory axis that impairs metabolic flexibility in obesity, which is a potential therapeutic target.
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