Individuals with anorexia nervosa present severe metabolic disturbances as a consequence of abnormal eating behaviors. Alterations in biochemical parameters have been described in AN (cortisol, cholesterol, electrolytes, etc.). However, the metabolic phenotype or fingerprinting of AN has been scarcely studied. Predominantly, plasma and serum samples are analyzed due to the ease of sample acquisition and the information they provide about the metabolic status. Generally, studies are focused on small groups of metabolites such as amino acids, lipids, or carbohydrates. Hence, wide untargeted metabolomics analyses are still lacking in AN. The main metabolomics alterations found in plasma from AN patients are summarized in
and detailed below.
Figure 1. Summary of the main metabolomic alterations found in plasma or serum samples from AN patients in the included studies. Altered pathways: (A) glycolysis and gluconeogenesis, (B) methionine and cysteine metabolism, (C) serine and glycine metabolism, (D) lipid metabolism, (E) urea cycle, (F) tricarboxylate cycle, (G) phenylalanine and tyrosine metabolism, (H) glutamate, glutamine, proline and histidine metabolism, (I) branched-chain amino acids metabolism, (J) serotonin pathway, (K) kynurenine pathway, (L) indole pathway, (M) tryptophan metabolism. Metabolites: (1) glucose, (2) pyruvate, (3) alanine, (4) taurine, (5) serine, (6) glycine, (7) methionine, (8) citrate, (9) cis-aconitate, (10) isocitrate, (11) succinate, (12) malate, (13) asparagine, (14) ornithine, (15) arginine, (16) guanidinosuccinate, (17) p-cresyl sulfate, (18) tyrosine, (19) phenylalanine, (20) phenylacetylglutamine, (21) phenylacetate, (22) hippurate, (23) tryptophan, (24) indole-3-acetate, (25) indoxyl sulfate, (26) glutamate, (27) glutamine, (28) histidine, (29) proline, (30) fatty acids, (31) phosphatidylcholines, (32) lysophosphatidylcholines, (33) sphingomyelins, (34) acylcarnitines, (35) oxylipins, (36) leucine, (37) isoleucine.