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J Neurochem (2012) 122(1):2219.10.1111/j.1471-4159.2012.07763.x 24 BorkumJM

Leu, Ile, and Val) in macrophages can not only replenish TCA cycle-related intermediates through BCAT/BCKDH-mediated catabolism, but also influence inflammation-related transcriptional programs through transport and nutrient-sensing pathways, such as mechanistic target of mTORC1 ( The regulatory features of BCAAs in macrophage polarization are mainly reflected in their role as an intersection node linking nutrient sensing-mTOR signaling-energy metabolic coupling. After entering cells, BCAAs can be converted by BCAT into branched-chain -keto acids, which are further catabolized by the BCKDH complex to generate products such as acetyl-CoA, succinyl-CoA, or propionyl-CoA, thereby connecting to the supply of TCA cycle intermediates and mitochondrial oxidative metabolism ( Current studies suggest that the effects of BCAAs on macrophage phenotypes are markedly context-dependent and may show bidirectional outcomes across different experimental systems

Udenfriend S, Wyngaarden JB (1956) Precursors of adrenal epinephrine and norepinephrine in vivo

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