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Significance Overnutrition leads to metabolic disorders including obesity and diabetes. Studies have shown that enhanced inflammation is an essential player in the progression of metabolic diseases. However, how immune cells sense nutritional status and contribute to whole-body metabolism are largely unknown. ProteinO -linked β-N -acetylglucosamine (O -GlcNAc) modification is thought to be a metabolic sensor that modulates cell signaling. Here, we show that overnutrition stimulatesO -GlcNAc signaling in macrophages.O -GlcNAc signaling suppresses macrophage proinflammatory activation and protects against diet-induced obesity and metabolic dysfunction. This study uncoversO -GlcNAc signaling as a homeostatic regulator at the interface of inflammation and metabolism and suggests thatO -GlcNAc signaling may serve as a therapeutic target for obesity, diabetes, and other immune-related diseases.

OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance