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Instead, approaches to reduce the risks associated with this dietary habit are more reasonable

[38] [36] -KIC is mostly metabolized by the mitochondrial enzyme branched-chain -ketoacid dehydrogenase, which converts it to isovaleryl-CoA

However, this compound can also be absorbed by macrophages during the formation of atherosclerotic plaque, with TMAO molecules binding to specific receptors on the surface of the macrophages, which triggers a series of signaling events inside the cell that activate specific pathways that induce the expression of genes involved in cholesterol metabolism, inflammation, and oxidative stress (77, 78)

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This is predominantly associated with rearrangement of HDLs aqueous phase and surface area (767)