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For example, -KG supplementation can promote the transition of macrophages from M1 to M2/reparative phenotypes and improve disease activity in colitis models (123), providing support for the clinical research hypothesis of nutrition-metabolic anaplerosis-immune repair. Lowering circulating BCAA levels can inhibit M1 polarization, and modulation of their metabolic enzymes has become a therapeutic strategy in patients with obesity and insulin resistance (42, 124)

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