Abstract
We hypothesized that sphingolipids may be early biomarkers of gestational diabetes mellitus (GDM). Here, 520 women with normal fasting plasma glucose levels were recruited in the first trimester and tested with a 75 g oral glucose tolerance test in the 24th–28th week of pregnancy. Serum sphingolipids concentrations were measured in the first and the second trimester by ultra-high performance liquid chromatography coupled with triple quadrupole mass spectrometry (UHPLC/MS/MS) in 53 patients who were diagnosed with GDM, as well as 82 pregnant women with normal glucose tolerance (NGT) and 32 non-pregnant women. In the first trimester, pregnant women showed higher concentrations of C16:0, C18:1, C22:0, C24:1, and C24:0-Cer and lower levels of sphinganine (SPA) and sphingosine-1-phosphate (S1P) compared to non-pregnant women. During pregnancy, we observed significant changes in C16:0, C18:0, C18:1, and C24:1-Cer levels in the GDM group and C18:1 and C24:0-Cer in NGT. The GDM (pre-conversion) and NGT groups in the first trimester differed solely in the levels of C18:1-Cer (AUC = 0.702 p = 0.008), also considering glycemia. Thus, C18:1-Cer revealed its potential as a GDM biomarker. Sphingolipids are known to be a modulator of insulin resistance, and our results indicate that ceramide measurements in early pregnancy may help with GDM screening.
Highlights
Gestational diabetes mellitus (GDM) is defined as glucose intolerance first recognized during pregnancy
Data are shown as medians; ◦ differences between all groups were analyzed by Kruskal–Wallis test. * The difference between normal glucose tolerance (NGT) and GDM groups was compared by Mann–Whitney U test
The data show that the main pathophysiological dysfunction in GDM is the increasing insulin resistance and insufficient insulin compensation, usually as a result of the β-cell impairment [1,22]
Summary
Gestational diabetes mellitus (GDM) is defined as glucose intolerance first recognized during pregnancy It is usually the result of β-cell dysfunction on a background of chronic insulin resistance [1]. We observe an increase in lipid concentration, especially in triglycerides, and, to a lesser extent, phospholipids and cholesterol It is the result of altered maternal metabolism [5]. Available data suggest that it is a major contributing factor of insulin resistance in skeletal muscles and the liver [13,14,15] These compounds induce insulin resistance at the level of RACα serine/threonine-protein kinase, known as Akt or protein kinase B-PKB [16]. ApoM-S1P has been shown to inhibit inflammatory responses in endothelial cells [18] These features suggest that S1P may induce the disorders leading to GDM, but there is little literature data on this subject. Serum sphingolipid levels were measured in the first and the second trimester and compared between the patients with normal glucose tolerance (NGT) and GDM diagnosed between 24 and 28 weeks of pregnancy
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