Serum concentration of zinc is elevated in clinically stable bipolar disorder patients.


Journal

Brain and behavior
ISSN: 2162-3279
Titre abrégé: Brain Behav
Pays: United States
ID NLM: 101570837

Informations de publication

Date de publication:
01 2022
Historique:
revised: 06 11 2021
received: 04 07 2021
accepted: 01 12 2021
pubmed: 31 12 2021
medline: 15 3 2022
entrez: 30 12 2021
Statut: ppublish

Résumé

Bipolar disorder (BD) is a chronic psychiatric disorder characterized by recurrent mood episodes interspersed with euthymic periods. A growing number of studies have indicated that zinc plays an important role in coordinating immune responses, as well as being involved in synaptic transmission. In the current study, we set out to measure serum levels of zinc in a meticulously phenotyped cohort of 121 euthymic BD subjects and 30 matched controls. Serum levels of zinc were measured by photometry. To assess the interplay between zinc levels and immune activation in BD, we measured serum levels of high-sensitive C-reactive protein (hsCRP) levels by immunoturbidimetric assay, and serum levels of monocyte chemoattractant protein-1 (MCP-1), chitinase 3-like protein 1 (YKL-40), and soluble cluster of differentiation 14 (sCD14) by electrochemiluminescence enzyme-linked immunosorbent assays. The baseline clinical diagnostic instrument for BD was the Affective Disorder Evaluation, and executive functioning was assessed by using the Delis-Kaplan Executive Function System. Controlling for potential confounding factors, BD patients displayed increased serum levels of zinc unrelated to hsCRP, MCP-1, YKL-40, and sCD14 levels. Serum levels of zinc did not associate with executive functioning or measurements of disease severity. This study suggests that the zinc homeostasis is disturbed in BD and that this dyshomeostasis is not related to ongoing mood symptoms or immune activation. Of note, serum levels were increased and hence do not support continuous zinc supplementation in BD.

Sections du résumé

BACKGROUND
Bipolar disorder (BD) is a chronic psychiatric disorder characterized by recurrent mood episodes interspersed with euthymic periods. A growing number of studies have indicated that zinc plays an important role in coordinating immune responses, as well as being involved in synaptic transmission. In the current study, we set out to measure serum levels of zinc in a meticulously phenotyped cohort of 121 euthymic BD subjects and 30 matched controls.
METHODS
Serum levels of zinc were measured by photometry. To assess the interplay between zinc levels and immune activation in BD, we measured serum levels of high-sensitive C-reactive protein (hsCRP) levels by immunoturbidimetric assay, and serum levels of monocyte chemoattractant protein-1 (MCP-1), chitinase 3-like protein 1 (YKL-40), and soluble cluster of differentiation 14 (sCD14) by electrochemiluminescence enzyme-linked immunosorbent assays. The baseline clinical diagnostic instrument for BD was the Affective Disorder Evaluation, and executive functioning was assessed by using the Delis-Kaplan Executive Function System.
RESULTS
Controlling for potential confounding factors, BD patients displayed increased serum levels of zinc unrelated to hsCRP, MCP-1, YKL-40, and sCD14 levels. Serum levels of zinc did not associate with executive functioning or measurements of disease severity.
DISCUSSION
This study suggests that the zinc homeostasis is disturbed in BD and that this dyshomeostasis is not related to ongoing mood symptoms or immune activation. Of note, serum levels were increased and hence do not support continuous zinc supplementation in BD.

Identifiants

pubmed: 34967503
doi: 10.1002/brb3.2472
pmc: PMC8785612
doi:

Substances chimiques

C-Reactive Protein 9007-41-4
Zinc J41CSQ7QDS

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2472

Informations de copyright

© 2021 The Authors. Brain and Behavior published by Wiley Periodicals LLC.

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Auteurs

Bo H Jonsson (BH)

Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm & Stockholm Health Care Services, Stockholm County Council, Karolinska Institutet, Stockholm, Sweden.

Funda Orhan (F)

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Sanna Bruno (S)

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Ana Osório Oliveira (AO)

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Timea Sparding (T)

Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.

Mikael Landen (M)

Section of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Carl M Sellgren (CM)

Department of Clinical Neuroscience, Centre for Psychiatry Research, Stockholm & Stockholm Health Care Services, Stockholm County Council, Karolinska Institutet, Stockholm, Sweden.
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

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