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Table 1 Metabolic pathways in macrophages

From: Metabolic reprogramming in macrophage responses

  M1/M[LPS(±IFNγ)] M2/M[IL-4/IL-10] Contradictory observations
Arginine metabolism Metabolized arginine to NO and citrulline by iNOS (9) Hydrolyzed arginine to ornithine and urea by arginase (9)  
Glycolysis Glycolysis is enhanced (21) Glycolysis is essential for M2 activation (11,34,36,37) Glycolysis does not affect M2 activation (38)
PPP Increased PPP pathway, providing NADPH for the production of ROS and NO (25,41) Upregulation of CARKL, which is contributed to the suppression of PPP (41)  
OXPHOS Reduced OXPHOS (21) with the conditions of high mitochondrial membrane potential, M1 leads to reversal of the normal direction of electron flow causing RET at complex I, driving ROS production (56) High OXPHOS (21,34)  
TCA cycle Broken in two places — after citrate and after succinate (40) An intact TCA cycle (40)  
FAS FAS is increased and is contributed to the pro-inflammatory responses (60-62) FAS fuels of FAO in M2 activation (37)  
FAO   Enhanced FAO is contributed to the activation of M2 (65,66) FAO is not essential during the M2 activation (67,69)
Glutamine metabolism Glutamine can replesh succinate through “GABA shunt” and anaplerosis from a-ketoglutarate, and promotes the inflammatory response of macrophages (53) Glutamine is contributed to the M2 activation (40,71) Transiently deprived macrophage of glutamine has no effect for M1 polarization (40)