Indoleacetic Acid

Optimal result: 0 – 4.2 mmol/mol creatinine

Elevated IAA in the urine suggests incomplete digestion and absorption of tryptophan in the intestine, allowing colonic bacteria to convert tryptophan to IAA. Elevations may also reflect an overgrowth of bacteria acting on tryptophan.

Clinical Associations: IAA elevations and altered tryptophan metabolism have been associated with systemic inflammation, psychologic and cognitive function, autism, and chronic diseases such as cardiovascular disease. Hartnup’s disease, a genetically-linked dysfunction in the transport of freeform amino acids across the intestinal mucosa, can cause severe elevations of urinary IAA.

Indoleacetic acid (IAA), or indole-3-acetate, is produced by the bacterial fermentation of the amino acid tryptophan.

IAA can be formed from several common gut microbes such as Clostridia species, Escherichia coli, and Saccharomyces species.

Indoleacetic acid (IAA), or indole-3-acetate, is produced by the bacterial fermentation of the amino acid tryptophan.

IAA can be formed from several common gut microbes such as Clostridia species, Escherichia coli, and Saccharomyces species.

Common Dietary Sources:

High tryptophan intake, green/black tea

References:

- Blaut M, Clavel T. Metabolic Diversity of the Intestinal Microbiota: Implications for Health and Disease. J Nutr. 2007;137(3):751S-755S.

- Russell WR, Duncan SH, Scobbie L, et al. Major phenylpropanoidderived metabolites in the human gut can arise from microbial fermentation of protein. Mol Nutr Food Res. 2013;57(3):523-535.

- Rao RP, Hunter A, Kashpur O, Normanly J. Aberrant synthesis of indole-3-acetic acid in Saccharomyces cerevisiae triggers morphogenic transition, a virulence trait of pathogenic fungi. Genetics. 2010;185(1):211-220.

- Evenepoel P, Meijers BKI, Bammens BRM, Verbeke K. Uremic toxins originating from colonic microbial metabolism. Kidney Int.76:S12-S19.

- Karu N, McKercher C, Nichols DS, et al. Tryptophan metabolism, its relation to inflammation and stress markers and association with psychological and cognitive functioning: Tasmanian Chronic Kidney Disease pilot study. BMC Nephrol. 2016;17(1):171.

- Sallée M, Dou L, Cerini C, Poitevin S, Brunet P, Burtey S. The Aryl Hydrocarbon Receptor-Activating Effect of Uremic Toxins from Tryptophan Metabolism: A New Concept to Understand Cardiovascular Complications of Chronic Kidney Disease. Toxins. 2014;6(3):934-949.

- Gevi F, Zolla L, Gabriele S, Persico AM. Urinary metabolomics of young Italian autistic children supports abnormal tryptophan and purine metabolism. Mol Autism. 2016;7:47.

- Wong PW, Lambert AM, Pillai PM, Jones PM. Observations on nicotinic acid therapy in Hartnup disease. Arch Dis Child. 1967;42(226):642-646.

Indoleacetic Acid
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