The metabolism of inflammation is regulated by AMPK and pseudo-starvation. Activated inflammatory cells, such as macrophages and T-helper 17 cells, exhibit increased glucose uptake, glycolysis, and pentose phosphate pathway activity. In contrast, anti-inflammatory cells like M2 macrophages and regulatory T cells have lower glycolysis and higher oxidative metabolism. Some anti-inflammatory agents may induce a pseudo-starvation state through AMPK activation. Metabolism is traditionally viewed as energy production, but recent studies show that metabolic changes are crucial in diseases like cancer and inflammation. Otto Warburg proposed that metabolic dysregulation is a feature of tumour cells, where glycolysis is preferred even in the presence of oxygen, known as the Warburg effect. Studies on activated macrophages began in the 1960s, showing increased glycolysis. In 1982, a study showed increased glycolysis and glutamine use in lymphocytes during immune activation. Activated macrophages have high hexokinase activity, and glycolysis and glutamine metabolism increase during phagocytosis. Recent studies confirm that macrophages and dendritic cells activated by lipopolysaccharide shift to aerobic glycolysis. In contrast, anti-inflammatory cells exhibit oxidative metabolism. Mechanistic insights into these changes involve HIF-1α and AMPK. The similarity between tumour and inflammatory cells is that both have metabolic changes driven by extracellular signals. Inflammation is energy-intensive, and activated macrophages switch to glycolysis, similar to tumour cells. The metabolism of activated T cells involves PI(3)K-Akt and mTOR pathways, as well as c-myc. Tumour cells have metabolic changes driven by mutations, while inflammatory cells are driven by extracellular signals. Dendritic cells switch to glycolysis upon TLR activation, with increased glucose transporter expression and lactate production. IL-10 limits this switch, suggesting a net anti-inflammatory effect. TLR4 activation increases ROS production, which is important for macrophage bactericidal activity. Macrophages activated by LPS and IFN-γ acquire an M1 phenotype with increased glycolysis and PFKFB3 expression. In contrast, macrophages activated by IL-4 and IL-13 acquire an M2 phenotype with increased oxidative phosphorylation and PFKFB1 expression. PGC-1β is key in the M2 phenotype, promoting fatty-acid oxidation and mitochondrial biogenesis. Sirtuins, NAD+-dependent deacetylases, are anti-inflammatory and promote a switch from glycolysis to fatty-acid oxidation. Sirt1 deacetylates and inactivates NF-κB, limiting its expression. Sirt1 also activates PGC-1β, promoting fatty-acid oxidation. CARKL is a key driver of the M2 phenotype,The metabolism of inflammation is regulated by AMPK and pseudo-starvation. Activated inflammatory cells, such as macrophages and T-helper 17 cells, exhibit increased glucose uptake, glycolysis, and pentose phosphate pathway activity. In contrast, anti-inflammatory cells like M2 macrophages and regulatory T cells have lower glycolysis and higher oxidative metabolism. Some anti-inflammatory agents may induce a pseudo-starvation state through AMPK activation. Metabolism is traditionally viewed as energy production, but recent studies show that metabolic changes are crucial in diseases like cancer and inflammation. Otto Warburg proposed that metabolic dysregulation is a feature of tumour cells, where glycolysis is preferred even in the presence of oxygen, known as the Warburg effect. Studies on activated macrophages began in the 1960s, showing increased glycolysis. In 1982, a study showed increased glycolysis and glutamine use in lymphocytes during immune activation. Activated macrophages have high hexokinase activity, and glycolysis and glutamine metabolism increase during phagocytosis. Recent studies confirm that macrophages and dendritic cells activated by lipopolysaccharide shift to aerobic glycolysis. In contrast, anti-inflammatory cells exhibit oxidative metabolism. Mechanistic insights into these changes involve HIF-1α and AMPK. The similarity between tumour and inflammatory cells is that both have metabolic changes driven by extracellular signals. Inflammation is energy-intensive, and activated macrophages switch to glycolysis, similar to tumour cells. The metabolism of activated T cells involves PI(3)K-Akt and mTOR pathways, as well as c-myc. Tumour cells have metabolic changes driven by mutations, while inflammatory cells are driven by extracellular signals. Dendritic cells switch to glycolysis upon TLR activation, with increased glucose transporter expression and lactate production. IL-10 limits this switch, suggesting a net anti-inflammatory effect. TLR4 activation increases ROS production, which is important for macrophage bactericidal activity. Macrophages activated by LPS and IFN-γ acquire an M1 phenotype with increased glycolysis and PFKFB3 expression. In contrast, macrophages activated by IL-4 and IL-13 acquire an M2 phenotype with increased oxidative phosphorylation and PFKFB1 expression. PGC-1β is key in the M2 phenotype, promoting fatty-acid oxidation and mitochondrial biogenesis. Sirtuins, NAD+-dependent deacetylases, are anti-inflammatory and promote a switch from glycolysis to fatty-acid oxidation. Sirt1 deacetylates and inactivates NF-κB, limiting its expression. Sirt1 also activates PGC-1β, promoting fatty-acid oxidation. CARKL is a key driver of the M2 phenotype,