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Systemic concentration of apelin, but not resistin or chemerin, is altered in patients with schizophrenia
  1. Elżbieta Kozłowska1,
  2. Ewa Brzezińska-Błaszczyk1,
  3. Adam Wysokiński2,
  4. Paulina Żelechowska1
  1. 1 Department of Experimental Immunology, Medical University of Lodz, Lodz, Lodzkie, Poland
  2. 2 Department of Old Age Psychiatry and Psychotic Disorders, Medical University of Lodz, Lodz, Lodzkie, Poland
  1. Correspondence to Dr Elżbieta Kozłowska, Department of Experimental Immunology, Medical University of Lodz, Lodz 92-213, Lodzkie, Poland; elzbieta.kozlowska{at}umed.lodz.pl

Abstract

It has been suggested that immune-inflammatory processes might be involved in the etiopathogenesis of schizophrenia. Since growing evidence indicates that adipokines strongly modulate the course of immune response and inflammatory processes, it is currently suggested the contribution of those factors in the etiology of schizophrenia as well. The aim of this study was to determine the serum levels of 4 adipokines—apelin, resistin, chemerin, and omentin—in patients with schizophrenia as compared with healthy subjects. Fifty-seven adult patients with schizophrenia and 31 healthy volunteers were included in this prospective study. ELISA was used to measure the serum concentration of resistin, apelin, omentin-1, and chemerin. No difference in the mean concentration of resistin (p=0.20) and chemerin (p=0.30) between patients with schizophrenia and the healthy group was observed. Apelin concentration was significantly (p=0.004) lower in patients with schizophrenia as compared with controls. A significant difference in apelin level between men with schizophrenia and control group (p=0.04) was reported. Apelin concentration was significantly correlated with waist-to-hip ratio, whereas chemerin concentration was significantly correlated with the Positive and Negative Syndrome Scale G score. There exists evidence that apelin might be involved in the pathogenesis of schizophrenia.

  • schizophrenia
  • adipokines
  • body composition
  • inflammation

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Footnotes

  • Contributors EK, AW, EBB and PŻ conceived and designed the experiments. AW and EK collected the sample information. EK and PŻ performed the experiments. EK, AW, and PŻ analyzed the data. EK, PŻ, AW, and EBB wrote the manuscript.

  • Funding This study was financially supported by the Medical University of Lodz (grant numbers 503/6-164-01/503-61-001 and 503/6-164-01/503-66-001).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval The study protocol was approved by the Bioethics Commission of the Medical University of Lodz (RNN/122/16/KE). The investigation was carried out in accordance with the latest version of the Declaration of Helsinki.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement The data used to support the findings of this study are included within the article.

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