Identification of endogenous acyl amino acids based on a targeted lipidomics approach

Increased Glucose Metabolism and Glycerolipid Formation by Fatty Acids and GPR40 Receptor Signaling Underlies the Fatty Acid Potentiation of Insulin Secretion

“…These fatty acid derivatives have not been reported previously in ␤ cells, and their effect is unknown. Acylamides have been found in neuronal tissue and reportedly possess various functions (34,35), including modulation of calcium flux, nitric oxide generation (36), and transient receptor potential (TRP) calcium channels (37). Although we were able to increase the intracellular concentration of those metabolites by increasing the levels of their amino acid precursors, this did not result in alterations in insulin secretion.…”

Self-assembly, supramolecular organization, and phase transitions of a homologous series of N-acyl-l-alanines (n=8–20)

“…Recent research indicates that N-acyl amino acids and N-acyl neurotransmitters (NAANs) are emerging as a new class of lipid mediators with significant biological functions [2][3][4][5][6][7]. So far, more than 70 NAANs have been identified in the mammals [8].…”

Clostridium difficile heterogeneously impacts intestinal community architecture but drives stable metabolome responses

“…Briefly, six putatively identified metabolites (Leonuriside A, N-palmitoyl glutamic acid, phlorizin, two tripeptides and ceramide) were C. difficile specific (Figure 3), as they were found in patients with CDAD regardless of toxin production, but not in non-colonised control patients (P-value ≤ 0.0152). These chemicals are implicated in the regulation of chronic intestinal inflammation, cell growth and signal transduction (Qiu et al, 1996;Lauzon et al, 2003;Tan et al, 2010;Kurek et al, 2013). They also function as binding sites for bacteria and their toxins to prevent the translocation of pathogens (Kurek et al, 2013).…”

“…They include (i) two fatty acids, 22 lipids (including gluco-, glycero-and glycerophospho-lipids) and 10 bile acid derivatives, low levels of which have been reported to promote cell lipotoxicity and apoptosis and have an overall cathartic effect on the colon (Yoon et al, 2002;Senkal et al, 2011;Swann et al, 2011;Longato et al, 2012); (ii) five N-acyl amino acids or polyamides (including arachidoyl glycine, N-stearoyl proline, N-oleoyl (iso)leucine, N-stearoyl tyrosine and N-palmitoyl threonine), the absence of which promotes dysfunction in the regulation of host temperature, locomotion and inflammation (Tan et al, 2010); (iii) ferroxamine and five metabolites implicated in porphyrin and iron metabolism, the deficiency of which decreases the concentration of beneficial gut microbiota and induces iron deficiency anaemia (Dostal et al, 2014); (iv) 12 presumptive secondary metabolites and bioactive peptides, such as methionine enkephalin and a number of tripeptides, the metabolism failure of which has been shown to lead to failure in immune and neuroactive ligand-receptor interactions (Yoshimasa et al, 1982;Salzet and Tasiemski, 2001); (v) inosine, pseudouridine and hypoxanthine, nucleoside and purine derivatives, the depletion of which may negatively influence the initiation of translation and nucleic acid synthesis in human gut microbiota and in gut mucosal defence (Grimble, 1994); and (vi) six ceramide/sphingolipid derivatives, creatinine, N-acetylhistamine, glyoxylate and succinate-ceramide and creatinine deficits in the gut have been associated with liver and renal dysfunctions (Peral et al, 2002; Longato et al, . Notably, the production of the above metabolites was observed in patients carrying toxin + C. difficile strains (Supplementary Table 2).…”