The article discusses the metabolic changes in cells involved in inflammation, such as activated macrophages and T-helper 17 (Th17) cells, which include enhanced glucose uptake, glycolysis, and increased activity of the pentose phosphate pathway. In contrast, anti-inflammatory cells like M2 macrophages, regulatory T cells, and quiescent memory T cells exhibit lower glycolytic rates and higher oxidative metabolism. The role of hypoxia-inducible factor 1α (HIF-1α) and AMP-activated protein kinase (AMPK) in these metabolic changes is proposed. AMPK activation can induce a pseudo-starvation state by promoting mitochondrial metabolism and fatty acid oxidation, potentially acting as a therapeutic target for inflammatory diseases. The article also highlights the importance of sirtuins and carbohydrate kinase-like protein (CARKL) in regulating macrophage metabolism and inflammation. Additionally, it explores the metabolic differences between M1 and M2 macrophages, Th17 and regulatory T (Treg) cells, and CD8+ memory T cells, emphasizing the role of HIF-1α in inflammation and the potential of AMPK activators as anti-inflammatory agents.The article discusses the metabolic changes in cells involved in inflammation, such as activated macrophages and T-helper 17 (Th17) cells, which include enhanced glucose uptake, glycolysis, and increased activity of the pentose phosphate pathway. In contrast, anti-inflammatory cells like M2 macrophages, regulatory T cells, and quiescent memory T cells exhibit lower glycolytic rates and higher oxidative metabolism. The role of hypoxia-inducible factor 1α (HIF-1α) and AMP-activated protein kinase (AMPK) in these metabolic changes is proposed. AMPK activation can induce a pseudo-starvation state by promoting mitochondrial metabolism and fatty acid oxidation, potentially acting as a therapeutic target for inflammatory diseases. The article also highlights the importance of sirtuins and carbohydrate kinase-like protein (CARKL) in regulating macrophage metabolism and inflammation. Additionally, it explores the metabolic differences between M1 and M2 macrophages, Th17 and regulatory T (Treg) cells, and CD8+ memory T cells, emphasizing the role of HIF-1α in inflammation and the potential of AMPK activators as anti-inflammatory agents.