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Atherosclerotic cardiovascular disease is caused by proinflammatory stimuli in the vascular endothelial cells and is associated with increased plasma levels of TNF- , IL-6, CRP, and circulating endotoxin (i.e., lipopolysaccharide (LPS)) [56, 57]

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Last, Gln enters cells by exchange with leucine (Leu) and activates the mammalian target of rapamycin (mTOR) [8], which further regulates lipid synthesis, nucleotide synthesis, and glucose metabolism