Maternal lipids, BMI and IL‑17/IL‑35 imbalance in concurrent gestational diabetes mellitus and preeclampsia

Abstract

The objective of the present study was to investigate the role of blood glucose, lipid metabolism, body mass index (BMI), C-reactive protein (CRP) as well as an interleukin (IL)-17/IL-35 imbalance in the pathogenesis of concurrent gestational diabetes mellitus (GDM) and preeclampsia (PE) (DPE). The mRNA expression of forkhead box protein 3 (FoxP3), IL-35 [including Epstein-Barr virus-induced gene 3 (EBI3) and P35 subunits] and IL-17 in the peripheral blood mononuclear cells of patients with DPE (n=30), GDM (n=33), PE (n=33) and normal pregnancy (n=33) were determined by reverse transcription-quantitative polymerase chain reaction. The serum levels of IL-35, IL-17 and CRP were analyzed using ELISA. Serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) and fasting blood glucose (FBG) were also detected. The levels of low-density lipoprotein (LDL) were calculated using the Friedewald formula. Body weight and height were determined in order to calculate the BMI. It was observed that the levels of FBG were markedly elevated in patients with GDM, PE and DPE. In addition, significantly higher serum TG, TC, LDL and very LDL were detected in patients with GDM, PE and DPE compared with those in subjects with normal pregnancies. By contrast, the concentration of HDL was lower in the patient groups. In addition, higher BMI values were identified in patients with GDM, PE and DPE. A decreased expression of FoxP3, P35 and EBI3 mRNA, and an elevated expression of IL-17 in PBMCs was detected in patients with GDM, PE and DPE. In addition, higher serum levels of IL-17 and CRP, as well as lower levels of IL-35, were observed. Furthermore, in patients with DPE, positive correlations of diastolic blood pressure with IL-17 levels, BMI and TG, as well as IL-17 levels with BMI and proteinuria were identified. In conclusion, the present study indicated that abnormal maternal lipids, hyperglycemia, high BMI, high CRP and IL-17/IL-35 imbalance may have a role in the pathophysiology of DPE. Therefore, pregnant women and clinicians should be made aware that maternal hyperlipidaemia, hyperglycemia, high BMI, high CRP levels and IL-17/IL-35 imbalance may lead to DPE.

A Study of the Association Between IL-17 and HOMA-IR in Iraqi Type 2 Diabetic Patients

“…Our results showed that there was a weak positive correlation of serum level of IL-17 with TG and VLDL in T2DM patient and the control groups. A previous study reported that elevated serum levels of IL-17, TG, and VLDL may play a role in the development of endothelial damage and vascular dysfunction, then causing systemic inflammation and endothelial dysfunction and may be involved in the pathogenesis of DM [31].…”

The application of metabolomics analysis in the research of gestational diabetes mellitus and preeclampsia

“…Lipid metabolism disorders begin in the early stages of the disease and play an important role in the development of metabolic diseases during pregnancy. 13,15 As the abnormal lipid metabolism can promote the incidence of GDM and/or PE, controlling blood lipids within an appropriate range may reduce the incidence of maternal complications. 16 Lysophosphatidylcholine LPC is increasingly recognized as a key factor positively associated with cardiovascular diseases.…”

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

“…Yan et al [9] demonstrated that serum and vitreous levels of IL-35 were significantly decreased in patients with proliferative diabetic retinopathy (PDR). Lower serum levels of IL-35 were also detected in patients with gestational diabetes mellitus (GDM) and preeclampsia (PE) [10]. A large quantity of evidence has revealed that IL-35 could inhibit tumor necrosis factor (TNF)-α-induced activation of nuclear factor (NF)-κB via the signal transducer and activator of transcription 1 (STAT1) phosphorylation and suppressed the phosphorylation of MAPK family including JNK, ERK, and p38 activated by lipopolysaccharide (LPS) [11, 12].…”