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. 2012 Jun 26;8:558. doi: 10.1038/msb.2012.21

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Copyright © 2012, EMBO and Macmillan Publishers Limited

This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial No Derivative Works 3.0 Unported License, which permits distribution and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation or the creation of derivative works without specific permission.

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Randomized sampling elucidates intracellular mechanisms for observed macrophage activation and suppression. Tryptophan induces a shift to a ketogenic-like state, increasing metabolic usage of leucine and lysine. To balance the redox potential shift, there is a significantly greater use of the malate-aspartate shuttle, diverting glutamate from activation pathways. In addition, increased nucleotide synthesis shifts metabolic resources toward nucleotide intermediates PRPP and CRP. PRPP and CRP are produced from glutamine and glucose, respectively, diverting metabolic resources from nitric oxide, proline, putrescine, and ATP generation.