Vol 65, No 3 (2014)
Original paper
Published online: 2014-06-27

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The IL-6/IL-6R/sgp130 system and Th17 associated cytokines in patients with gestational diabetes

Mariusz Kuźmicki, Beata Telejko, Danuta Lipińska, Justyna Pliszka, Juliusz Wilk, Natalia Wawrusiewicz-Kurylonek, Anna Zielińska, Angelika Sobota, Adam Krętowski, Maria Górska, Jacek Szamatowicz
DOI: 10.5603/EP.2014.0023
Endokrynol Pol 2014;65(3):169-175.

Abstract

Introduction: Interleukin-6 (IL-6) is a pleiotropic cytokine which signals through a cell surface receptor complex consisting of a cognatereceptor subunit (IL-6R) and glycoprotein 130 (gp130), which is considered an antagonist to the IL-6R/IL-6 pathway. The aim of the present study was to assess IL-6/IL-6R/gp130 system and Th17 associated cytokines in different time points during and after pregnancy in women with gestational diabetes mellitus (GDM) and normal glucose tolerance (NGT).

Material and methods: Serum levels of IL-6, sIL6R, sgp130, IL-17 and IL-23 were measured in 91 women divided into three groups: GDMin the 24th–28th week of gestation (visit 1), NGT at the 1st visit and GDM in the 29th-32nd week, and NGT at both visits.

Results: The patients with GDM recognised at the 1st visit had significantly higher IL-6 (p = 0.02) and sgp130 (p = 0.03) concentrations than had the women with NGT, whereas the women with GDM diagnosed at the 2nd visit had elevated sIL-6R concentrations (p = 0.03). The patients with low sIL-6R but high sgp130 concentration had significantly higher glucose levels (p = 0.04) and lower IL-6 values (p = 0.04) than had the patients with low sIL-6R and sgp130 concentrations. IL-17 and IL-23 were detected in approximately one-third of the population studied. A trend towards higher IL-17 levels was observed in the subjects with GDM, but the differences were not significant.

Conclusions: Our results suggest that an increased serum sgp130 concentration in the patients with GDM might represent a compensatory mechanism, controlling intracellular IL-6 signalling and preventing the activation of the IL-6/IL-6R pathway.