Fig 5. Infection causes a large shift in host metabolism as measured by whole blood metabolomics.

Creatine (A), a non-proteinogenic amino acid which is abundant in skeletal muscle and critical to energy metabolism, increased in concentration from BL the end of the experiments (End: *p = 0.01). The essential amino acid, phenylalanine (B), increased from baseline (BL) as systemic infection progressed (6h: ⁺p = 0.02; End: *p = 0.01). In parallel, the non-essential amino acid, tyrosine (C), that is produced from phenylalanine, also increased from BL (End: *p = 0.005). Lysine (D), an essential amino acid, progressively increased over the course of infection (End: *p = 0.0002). Inosine monophosphate (E), which is a nucleotide monophosphate, also progressively increased from BL (6h: ⁺p = 0.006; End: *p = 0.03). The essential amino acid, histidine (F), which is a precursor of histamine, was increased compared to BL at the end of the experiment (End: *p = 0.04). Consistent with the clinical measurement, glucose (G), progressively declined from BL to the end of the experiment (*p = 0.05). Glutamine (H), a non-essential amino acid, and methionine (I), an essential amino acid, both of which are important in maintaining glutathione homeostasis, were higher at the end of the experiments than at BL (End: *p = 0.006 and *p = 0.0001, respectively). Data are the mean(SE) of four animals. Metabolites are presented in ascending rank order of their FDR-corrected ANOVA p value which in all cases was less than 0.10. ⁺ Denotes significant difference between baseline and 6h. * Denotes significant difference between baseline and end of experiment.