Hostname: page-component-78c5997874-s2hrs Total loading time: 0 Render date: 2024-11-13T07:00:16.712Z Has data issue: false hasContentIssue false

Tryptophan metabolism in bipolar disorder

Published online by Cambridge University Press:  01 September 2022

F. Fellendorf*
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
M. Platzer
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
A. Birner
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
R. Queissner
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
S. Bengesser
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
M. Lenger
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
A. Maget
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
A. Tmava-Berisha
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
N. Dalkner
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
D. Fuchs
Affiliation:
Medical University Innsbruck, Institute Of Medical Biochemistry, Graz, Austria
J. Gostner
Affiliation:
Medical University Innsbruck, Institute Of Medical Biochemistry, Graz, Austria
E. Reininghaus
Affiliation:
Medical University Graz, Psychiatry And Psychotherapeutic Medicine, Graz, Austria
*
*Corresponding author.

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Introduction

Immune mediated inflammatory processes are involved in the aetiopathogenesis of bipolar disorder (BD) and weight associated comorbidities. Tryptophan breakdown via indoleamine 2,3-dioxygenase-1 (IDO-1) along the kynurenine axis concomitant with a pro-inflammatory state was found more active in BD but also associated with overweight/obesity.

Objectives

Aims of our study were to investigate 1.) the tryptophan metabolism in BD compared to mentally healthy controls, 2.) differences in weight classes, 3.) in a longitudinal setting, dependent on the incidence of BD episodes and euthymia.

Methods

At the Medical University Graz anthropometric and clinical data as well as peripheral tryptophan and kynurenine were assessed in serum samples of 226 individuals with BD and 142 controls. For 75 individuals with BD a longitudinal assessment with three samples was performed. Serum concentrations of tryptophan and kynurenine were determined by reverse-phase high-performance liquid chromatography. The kynurenine/tryptophan was used as a proxy for IDO-1 activity.

Results

showed a higher kynurenine/tryptophan ratio in BD compared to controls and in overweight compared to normal weight persons. Levels remained stable over time. In the longitudinal course, no differences were found between individuals who were constantly euthymic or not as well who had an illness episode or none.

Conclusions

Findings indicate that IDO-1 activity might constitute more a trait and not a state marker of BD. Accelerated tryptophan breakdown along the kynurenine axis may be further facilitated by overweight. This may increase the risk of accumulation of neurotoxic metabolites which impacts BD symptomatology, cognition, and somatic comorbidities.

Disclosure

No significant relationships.

Type
Abstract
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2022. Published by Cambridge University Press on behalf of the European Psychiatric Association
Submit a response

Comments

No Comments have been published for this article.