Adiposity-related inflammation: Effects of pregnancy

Authors

  • Camilla M. Friis,

    Corresponding author
    1. Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway
    • Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway

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  • Marie C. Paasche Roland,

    1. Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway
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  • Kristin Godang,

    1. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
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  • Thor Ueland,

    1. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
    2. Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway
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  • Tom Tanbo,

    1. Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway
    2. Faculty of Medicine, University of Oslo, Oslo, Norway
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  • Jens Bollerslev,

    1. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
    2. Faculty of Medicine, University of Oslo, Oslo, Norway
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  • Tore Henriksen

    1. Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway
    2. Faculty of Medicine, University of Oslo, Oslo, Norway
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  • Disclosure: The authors declared no conflicts of interest.

Abstract

In the nonpregnant population, there is extensive evidence of a systemic low-grade inflammatory status in relation to excess adipose tissue. Less is known about the relation during pregnancy.

Objective:

Our main objective was therefore to explore the effect of pregnancy on adiposity-related systemic inflammation.

Design and Methods:

This study is a longitudinal cohort study of 240 pregnant women of Scandinavian heritage at Oslo University hospital—Rikshospitalet, Norway from 2002 to 2005. The inflammatory markers (C-reactive protein [CRP], Interleukin-6 [IL-6], monocyte chemoattractant protein 1 [MCP-1], IL1-Ra, tumor necrosis factor receptor II, and IL-10) were measured at four timepoints during pregnancy and analyzed by enzyme immuno-assay. The women were categorized based on BMI at inclusion (BMI <25, 25–30, and >30 kg/m2). Data were analyzed by Friedman-test, Wilcoxon signed rank test, or Kruskal–Wallis test as appropriate.

Results:

Maternal adiposity was associated with significantly higher circulatory levels of several inflammatory markers (CRP, MCP-1, IL-6, and IL-1Ra). However, this proinflammatory upregulation was not evident toward the end of pregnancy, as levels of CRP, MCP-1, and IL-6 were not any longer significantly different between the BMI categories.

Conclusions:

Although normal pregnancy exhibits proinflammatory features, this does not seem to have additive or synergistic effects on the inflammation associated with adiposity. On the contrary, we found that the BMI-dependent increase in proinflammatory markers was not evident at the end of pregnancy.

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