4.2 Article

Regulation of Interleukin-6 and Leptin in Schizophrenia Patients: A Preliminary Analysis

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出版社

KOREAN COLL NEUROPSYCHOPHARMACOLOGY
DOI: 10.9758/cpn.2014.12.3.209

关键词

Inflammation; Immune; Psychotic disorders; Adipokines

资金

  1. National Medical Research Council, Singapore [NMRC/NIG/1017/2010]
  2. Singapore Ministry of Health's National Medical Research Council under its Transition Award [NMRC/TA/002/2012]

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Objective: Immune inflammatory mediators play a pivotal role in brain signaling and have been increasingly associated with the pathophysiology of schizophrenia. Many studies have indicated an increased level of immune inflammatory interleukin-6 (IL-6) in schizophrenia, IL-6 is a well known chief stimulator of inflammation, Of late leptin has also been implicated in the inflammatory pathway of schizophrenia. In this study we measured and compared serum levels of IL-6 and leptin in patients with schizophrenia to healthy controls, and investigated the relationship between IL-6 and leptin. Methods: Serum IL-6 and leptin were determined in 20 patients diagnosed with schizophrenia and in 19 healthy controls matched by gender, age and body mass index (BMI) using commercial Bioplex assays, Results: Using Mann-Whitney U-test, significantly increased IL-6 levels were found in the patients but there was no significant difference in leptin levels though a trend towards higher leptin was observed in the patients. Spearman correlations did not show any correlation between IL-6 and clinical variables except antipsychotic dosage. Leptin significantly correlated with gender and BMI. A large effect size correlation was observed between IL-6 and leptin in the patients but not in the controls, Multiple regression analysis performed on patients, after adjusting for gender and BMI, revealed there was no significant association between IL-6 and leptin. Conclusion: IL-6 and leotin levels may reflect the chronic inflammatory state associated with schizophrenia but further evaluation is required. Also, it is important to consider the confounding effects of obesity in any examination of relationships between groups with regard to cytokines and adipokines.

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