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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 α-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

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Here, rating scales are also used as outcome measures, with trials showing relatively modest effects compared to placebo [90,95]