High resistin and interleukin-6 levels are associated with gestational diabetes mellitus
Resistin is a cysteine-rich adipokine originally described as a molecular link between obesity and insulin resistance in rodents. In this study, we hypothesised that serum resistin concentrations are elevated in patients with gestational diabetes mellitus (GDM) when compared with pregnant women with...
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Published in: | Gynecological endocrinology Vol. 25; no. 4; pp. 258 - 263 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
Informa UK Ltd
01-04-2009
Taylor & Francis |
Subjects: | |
Online Access: | Get full text |
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Summary: | Resistin is a cysteine-rich adipokine originally described as a molecular link between obesity and insulin resistance in rodents. In this study, we hypothesised that serum resistin concentrations are elevated in patients with gestational diabetes mellitus (GDM) when compared with pregnant women with normal glucose tolerance (NGT) and related to proinflammatory interleukin-6 (IL-6) and other factors conferring insulin resistance. Serum resistin and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) in 81 women with GDM, 82 women with NGT between 24 and 31 weeks of gestation and 25 healthy non-pregnant women. Resistin concentrations were significantly higher in the GDM (21.9 [17.55-25.40] ng ml) than in the NGT group (19.03 [15.92-23.91] ng ml, p = 0.047), as well as in the non-pregnant women (14.8 [13.7-16.6] ng ml, p < 0.0001). Serum IL-6 levels were elevated in the GDM (1.0 [0.7-1.5] pg ml) as compared with the NGT group (0.8 [0.5-1.1] pg ml, p = 0.006) and the non-pregnant controls (0.7 [0.5-1.1] pg ml, p = 0.04). Multiple regression analysis revealed that in the pregnant women circulating resistin was related to serum IL-6 (β = 0.33, p = 0.0004) but not to insulin or the index of insulin resistance. It is concluded that the finding of high resistin and IL-6 levels in women with gestational diabetes might confirm a role of low-grade inflammation in the pathogenesis of GDM. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0951-3590 1473-0766 |
DOI: | 10.1080/09513590802653825 |