Indole-3-Propionic Acid, a Tryptophan-Derived Bacterial Metabolite, Reduces Weight Gain in Rats - PubMed (original) (raw)

Indole-3-Propionic Acid, a Tryptophan-Derived Bacterial Metabolite, Reduces Weight Gain in Rats

Piotr Konopelski et al. Nutrients. 2019.

Abstract

Recent evidence suggests that tryptophan, an essential amino acid, may exert biological effects by means of tryptophan-derived gut bacteria products. We evaluated the potential contribution of tryptophan-derived bacterial metabolites to body weight gain. The study comprised three experimental series performed on separate groups of male, Sprague-Dawley rats: (i) rats on standard laboratory diet treated with water solution of neomycin, an antibiotic, or tap water (controls-1); (ii) rats on standard diet (controls-2) or tryptophan-high (TH) or tryptophan-free (TF) diet; and (iii) rats treated with indole-3-propionic acid (I3P), a bacterial metabolite of tryptophan, or a vehicle (controls-3). (i) Rats treated with neomycin showed a significantly higher weight gain but lower stool and blood concentration of I3P than controls-1. (ii) The TH group showed significantly smaller increases in body weight but higher stool and plasma concentration of I3P than controls-2. In contrast, the TF group showed a decrease in body weight, decreased total serum protein and a significant increase in urine output. (iii) Rats treated with I3P showed significantly smaller weight gain than controls-3. Our study suggests that I3P, a gut bacteria metabolite of tryptophan, contributes to changes in body weight gain produced by antibiotics and tryptophan-rich diet.

Keywords: indoles; metabolism; microbiota; tryptophan; weight gain.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1

Figure 1

(A) Changes in body weight and (B) indole-3-propionic (I3P) acid concentration in plasma in Sprague Dawley rats treated with either neomycin, an antibiotic or water (controls) for 14 days. LQQ—below the limit of quantification; * p < 0.05 controls vs. neomycin. Means ± SE are presented, circles show individual data points.

Figure 2

Figure 2

(A) Changes in body weight and (B) indole-3-propionic acid (I3P) concentration in plasma in Sprague Dawley rats maintained on either standard laboratory chow (control), tryptophan-high chow (TH) or tryptophan-free chow (TF) for two weeks. * p < 0.05 vs. control; # p < 0.05 vs. TH, † p < 0.05 vs. TF. Means ± SE are presented, circles show individual data points.

Figure 3

Figure 3

(A) Changes in body weight during the experiment, (B) weight gain at the end of experiment, and (C) plasma indole-3-propionic acid (I3P) concentration at the end of experiment in Sprague Dawley rats treated with either indole-3-propionic acid (I3P group) or the vehicle (controls). * p < 0.05 vs. baseline, # p < 0.05 (time × group interaction) by ANOVA for repeated measurements, † p < 0.05 vehicle vs. I3P group. Means ± SE are presented, circles show individual data points.

References

    1. MacLean P.S., Blundell J.E., Mennella J.A., Batterham R.L. Biological control of appetite: A daunting complexity. Obesity (Silver Spring) 2017;25(Suppl. 1):8–16. doi: 10.1002/oby.21771. - DOI - PMC - PubMed
    1. Andermann M.L., Lowell B.B. Toward a Wiring Diagram Understanding of Appetite Control. Neuron. 2017;95:757–778. doi: 10.1016/j.neuron.2017.06.014. - DOI - PMC - PubMed
    1. Ufnal M., Drapala A., Sikora M., Zera T. Early high-sodium solid diet does not affect sodium intake, sodium preference, blood volume and blood pressure in adult Wistar-Kyoto rats. Br. J. Nutr. 2011;106:292–296. doi: 10.1017/S0007114511000110. - DOI - PubMed
    1. Broer S. The role of the neutral amino acid transporter B0AT1 (SLC6A19) in Hartnup disorder and protein nutrition. IUBMB Life. 2009;61:591–599. doi: 10.1002/iub.210. - DOI - PMC - PubMed
    1. Drummond K.N., Michael A.F., Good R.A. Tryptophan metabolism in a patient with phenylketonuria and scleroderma: A proposed explanation of the indole defect in phenylketonuria. Can. Med. Assoc. J. 1966;94:834–838. - PMC - PubMed

MeSH terms

Substances

LinkOut - more resources