Mediators of inflammation resolution and vasoactive eicosanoids in gestational diabetes and preeclampsia

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OBJECTIVE: Women with gestational diabetes (GDM) have an increased risk of preeclampsia and postpartum diabetes. Inflammation associates with both GDM and preeclampsia. This study examined specialized proresolving mediators (SPM) that direct inflammation resolution and eicosanoids that are involved in inflammation, in relation to the development of preeclampsia and ongoing postpartum glucose intolerance in GDM.

METHODS: Participants were selected from a prospective study examining the development of preeclampsia in women with GDM. Four groups of age-matched women were studied: GDM (n = 20), GDM who developed preeclampsia (GDM+PE, n = 21), GDM who remained glucose-intolerant postpartum (GDM+PPIGT, n = 20), or pregnancies with glucose tolerance within the normal range (NGT, n = 21). Measurement of SPM (E-series resolvins and D-series resolvins), SPM pathway intermediates (14-HDHA, 18-HEPE and 17-HDHA), 20-hydroxyeicosatetraenoic acid (20-HETE), and the urinary metabolite of the vasodilator prostacyclin 2,3-dinor-6-Keto-PGF1α, were made at 28, 32 and 36 weeks gestation and at 6 months postpartum.

RESULTS: Compared with GDM, GDM+PE had elevated levels of 20-HETE and the SPM pathway intermediates 14-HDHA, 18-HEPE, 17-HDHA, at 32 weeks, and the SPM RvE1 at 32 and 36 weeks gestation. Compared with NGT and regardless of whether they developed preeclampsia or PPIGT, GDM had lower levels of 2,3-dinor-6-Keto-PGF1α during pregnancy.

CONCLUSION: Reduced levels of the prostacyclin metabolite 2,3-dinor-6-Keto-PGF1α may contribute to the increased risk of preeclampsia in women with GDM. The increase in 20-HETE, a vasoconstrictor and mediator of inflammation, and SPM that contribute to inflammation resolution, prior to the onset of preeclampsia require further investigation to clarify their clinical significance.

Original languageEnglish
Pages (from-to)2236-2244
Number of pages9
JournalJournal of Hypertension
Issue number11
Publication statusPublished - 1 Nov 2022


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