Gestational diabesity and foetoplacental vascular dysfunction

Area of Science:

• Obstetrics and Gynecology
• Endocrinology
• Vascular Biology

Background:

• Gestational diabetes mellitus (GDM) involves impaired nutrient metabolism affecting the fetoplacental endothelium.
• Maternal hyperglycemia and hyperinsulinemia are key factors in GDM etiology, particularly in women with normal pre-pregnancy weight (classic GDM).
• Women with GDM and pre-pregnancy obesity (gestational diabesity, GDty) or overweight (GDMow) exhibit a distinct metabolic profile compared to classic GDM.

Purpose of the Study:

• To review the impact of GDty and GDMow on fetoplacental endothelial cell function.
• To highlight alterations in intracellular pH homeostasis, nitric oxide (NO) generation, and adenosine signaling.
• To underscore the need for differentiated metabolic characterization and therapeutic strategies for GDty/GDMow.

Main Methods:

• Literature review focusing on studies examining fetoplacental endothelial cell function in GDM subtypes.
• Analysis of metabolic differences between classic GDM, GDty, and GDMow.
• Examination of signaling pathways including l-arginine/nitric oxide and insulin/adenosine axes.

Main Results:

• GDty and GDMow are associated with altered l-arginine/nitric oxide and insulin/adenosine signaling in the fetoplacental endothelium.
• These alterations differ from those observed in classic GDM.
• Specific modulations in intracellular pH homeostasis and NO generation impact fetal vascular insulin resistance in GDty.

Conclusions:

• Women with GDty and GDMow possess a unique metabolic state distinct from classic GDM.
• The increasing prevalence of obesity necessitates recognizing these differences for targeted interventions.
• Developing specific therapeutic approaches for GDty and GDMow is crucial for maternal and fetal protection.