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New Insights into Tryptophan Metabolism
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New Insights into Tryptophan Metabolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 6354

Editor

Prof. Dr. Katsunori Nonogaki

E-Mail Website
Guest Editor
Division of Diabetes and Nutrition, Tohoku University, Sendai, Japan
Interests: bile acids; serotonin; serotonin receptor; Tph1; Tph2; tryptophan; tryptophan metabolites; GLP-1; GLP-1 receptor agonists; GIP; FGF21; FGF15/19; neuropeptides; gut-derived hormones; liver-derived hormones; obesity; diabetes; appetite; food intake; hypothalamus; energy homeosta-sis; hepatosteatosis; glucose metabolism; lipid metabolism; organ network; whey protein; soy protein; insulin; leptin; insulin resistance; adipose tissue; CNS; gene expression; sympathetic nervous system
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Special Issue Information

Dear Colleagues,

Tryptophan (Trp) is an essential amino acid that cannot be synthesized in the body and must be obtained via one's diet. In the body, Trp can be converted to serotonin (5-HT), kynurenine (Kyn), and indole-3-propionic acid (IPA). Trp and its metabolites are involved in health and a variety of diseases, including mental disorders, metabolic diseases, neurologic diseases, cardiovascular diseases, gastrointestinal diseases, immune diseases, and cancer.

Indoleamine-2,3 dioxygenase 1 (IDO1) is the enzyme responsible for converting Trp to Kyn. Tryptophan hydroxylase (Tph) is the enzyme responsible for converting Trp into 5-HT. Since the discovery of the two types of Tph (Tph1 and Tph2), it has become widely accepted that the central and peripheral 5-HT systems are functionally separate. Tph2 biosynthesizes 5-HT centrally, and Tph1 does so peripherally. A novel regulation of Trp and its metabolites, however, has recently been discovered: Tph1 can regulate Trp and its metabolites outside 5-HT in the plasma and brain.

In this Special Issue, we will explore novel regulatory mechanisms of Trp metabolism, novel functions of the rate-limiting enzymes for converting tryptophan, and the role of tryptophan metabolism in health and diseases. Any types of papers, including reviews, original papers, communications, and brief reports, are welcome.

Prof. Dr. Katsunori Nonogaki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tryptophan
  • serotonin
  • kynurenine
  • indole
  • metabolism
  • IPA
  • Tph
  • IDO1
  • health
  • disease

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Published Papers (2 papers)

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Review

35 pages, 2437 KB  
Review
The Kynurenine Pathway: Unraveling Its Role in Neurological Disorders via Mammalian Cellular Models
by Elizaveta S. Podshivalova, Sergey I. Kutsev and Aleksandr V. Shestopalov
Int. J. Mol. Sci. 2026, 27(14), 6337; https://doi.org/10.3390/ijms27146337 - 16 Jul 2026
Viewed by 554
Abstract
The kynurenine pathway (KP) constitutes the primary route of tryptophan catabolism, generating a spectrum of neuroactive metabolites that profoundly influence central nervous system function. Dysregulation of the KP is increasingly recognized as a critical pathogenic mechanism underlying diverse neuropathological conditions. This review critically [...] Read more.
The kynurenine pathway (KP) constitutes the primary route of tryptophan catabolism, generating a spectrum of neuroactive metabolites that profoundly influence central nervous system function. Dysregulation of the KP is increasingly recognized as a critical pathogenic mechanism underlying diverse neuropathological conditions. This review critically evaluates the most widely cited mammalian cellular models currently utilized to delineate the causal role of KP alterations in neurological disease. Specifically, this article examines primary cell cultures, immortalized and tumor-derived cell lines, stem cell-derived systems, and ex vivo organotypic brain slices and tissues, highlighting their distinct methodological advantages, translational limitations, and specific enzymatic profiles. Across the described cellular systems, a recurring mechanistic theme emerges: quinolinic acid-driven mitochondrial dysfunction, oxidative stress, and NAD+ depletion converge in neurodegenerative conditions such as Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Conversely, kynurenic acid exhibits disorder-dependent—and at times opposing—roles, attenuating dopaminergic neurotoxicity in Parkinson’s disease models while contributing to synaptic pruning deficits in schizophrenia models. Furthermore, cellular models demonstrate that IDO1/TDO induction and downstream metabolite shifts are frequently cell type- and species-dependent, complicating direct extrapolation to human pathology. Because no single experimental system achieves complete physiological fidelity, elucidating the complex dynamics of the KP and identifying novel therapeutic targets requires the integration of data across complementary platforms. Full article
(This article belongs to the Special Issue New Insights into Tryptophan Metabolism)
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49 pages, 2794 KB  
Review
Harnessing Dietary Tryptophan: Bridging the Gap Between Neurobiology and Psychiatry in Depression Management
by Amanda Chabrour Chehadi, Enzo Pereira de Lima, Cláudia Rucco Penteado Detregiachi, Rafael Santos de Argollo Haber, Virgínia Maria Cavallari Strozze Catharin, Lucas Fornari Laurindo, Vitor Engracia Valenti, Cristiano Machado Galhardi, Masaru Tanaka and Sandra Maria Barbalho
Int. J. Mol. Sci. 2026, 27(1), 465; https://doi.org/10.3390/ijms27010465 - 1 Jan 2026
Cited by 6 | Viewed by 4958
Abstract
Major depressive disorder remains a leading cause of disability worldwide, with conventional antidepressants offering incomplete and often transient relief. Mounting evidence highlights disturbances in tryptophan (Trp) metabolism as a key biological axis linking inflammation, neuroplasticity, and mood regulation. Plant-derived compounds that modulate this [...] Read more.
Major depressive disorder remains a leading cause of disability worldwide, with conventional antidepressants offering incomplete and often transient relief. Mounting evidence highlights disturbances in tryptophan (Trp) metabolism as a key biological axis linking inflammation, neuroplasticity, and mood regulation. Plant-derived compounds that modulate this pathway, including 5-hydroxytryptophan, isoflavones, berberine, and polyphenols, have emerged as promising candidates for integrative treatment strategies. Yet, despite encouraging preclinical and clinical findings, knowledge gaps persist regarding long-term efficacy, mechanistic specificity, and standardized therapeutic protocols. This narrative review explores how Trp modulators influence central and peripheral mechanisms relevant to depression, from serotonergic synthesis and kynurenine shunting to gut–brain–immune interactions. Evidence from animal models and randomized clinical trials is critically synthesized, with particular attention to outcomes on mood stabilization, anxiety reduction, cognitive function, and sleep regulation. Special emphasis is placed on translational potential, methodological limitations, and the need for harmonized research frameworks. Here we highlight that phytochemical interventions represent a mechanistically informed and biocompatible strategy for advancing depression management. By bridging neurobiology and clinical psychiatry, these insights may pave the way for next-generation therapeutics that integrate dietary, microbiota-targeted, and anti-inflammatory approaches. Broader application of this research could ultimately refine personalized psychiatry, expand therapeutic horizons, and contribute to global mental health resilience. Full article
(This article belongs to the Special Issue New Insights into Tryptophan Metabolism)
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