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Significance Emerging literature indicates that, besides circadian inputs, fed–fast cycles are vital for maintaining physiological homeostasis. While several studies have highlighted the importance of feeding and state-specific molecular signatures, information regarding mechanisms that bring about efficient fed–fast–refed transitions is sparse. Here we show how a glucose-derived modification (glycosylation) of SIRT1, a master regulator of transcription and insulin signaling, regulates this metabolic switch in the liver by restricting SIRT1 functions during fasted-to-refed transition. SIRT1 glycosylation orchestrates molecular interactions to suppress fasting genes, derepress fed genes, and activate insulin signaling upon refeeding. We show that aberrant SIRT1 glycosylation causes hepatic dysfunctions resulting in a diabetes-like state and is also associated with aging and obesity.

Spatiotemporal gating of SIRT1 functions by O-GlcNAcylation is essential for liver metabolic switching and prevents hyperglycemia