ArticleDiabetologia2026
Maternal pre-pregnancy BMI differentially regulates intracellular pH in human umbilical vein endothelium from gestational diabetes mellitus pregnancies, with alkalinisation-associated reduction of adenosine transport in normal weight pregnancies.
Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- A conceptual review of intracellular pH as a regulator of the adenosine-L-arginine-nitric oxide (ALANO) axis in human fetoplacental endothelial dysfunction in gestational diabetes mellitus.Pflugers Archiv : European journal of physiology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
aims/hypothesisGestational diabetes mellitus (GDM) is associated with fetoplacental endothelial dysfunction, including impaired extracellular clearance of adenosine, a vasodilator, in HUVECs. This study investigated the regulation of intracellular pH (pHi) and its impact on adenosine membrane transport in HUVECs. The hypothesis of this study was that Na
methodsHUVECs were isolated from 43 women with normal pregnancies and 23 with type A1 GDM and further stratified by maternal pre-pregnancy BMI into subgroups with normal weight, overweight and obesity. Data were also analysed as pooled groups (BMI ≥20 kg/m
resultsGDM was linked to intracellular alkalinisation (~0.6 pHi units vs normal pregnancies), increased activity of NHE1 and NHE isoforms 2 and 3 and reduced buffering capacity, with these effects varying by pre-pregnancy maternal BMI. Increased pHi recovery (~3.8-fold) and NHE1 activity (~4.8-fold) were observed in cells from women with GDM and pre-pregnancy overweight, while those with obesity (i.e. gestational diabesity) showed unaltered NHE1-mediated pHi recovery. Buffering capacity was reduced across most GDM groups, except in the overweight group. The GDM-reduced adenosine transport maximal capacity via human equilibrative nucleoside transporter isoform 2 was restored by intracellular acidification in GDM. CONCLUSIONS/
interpretationPre-pregnancy maternal metabolic status influences endothelial adaptation or maladaptation to GDM. Stratifying GDM cases by pre-pregnancy maternal BMI uncovers subgroup-specific physiological responses, highlighting the importance of tailored approaches in understanding GDM pathophysiology.
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