Extracellular vesicle-associated miR-515-5p from adipose tissue regulates placental metabolism and fetal growth in gestational diabetes mellitus

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Gestational diabetes mellitus (GDM) affects 2-20% of pregnant women worldwide and is linked to fetal overgrowth, increased perinatal morbidity, and mortality, as well as a higher risk of developing cardiovascular disease later in life for mother and child. MicroRNAs (miRNAs), which regulate gene expression, can be transported within extracellular vesicles (EVs). Adipose tissue-derived EVs have been associated with changes in placental metabolism in GDM, potentially influencing cardiovascular health outcomes. This study aimed to evaluate the miRNA profile in EVs from omental adipose tissue in GDM and their effect on placental nutrient uptake and fetal growth. Methods This case-control study included patients with normal glucose tolerance (NGT) and GDM. We conducted a miRNA expression profiling on omental adipose tissue and its derived EVs from women with NGT (n = 20) and GDM (n = 36). Trophoblast cells were utilized to assess the effect of EVs on glucose and fatty acid uptake, pro-inflammatory cytokine, and chemokine release. Double-stranded miRNA mimics were used to investigate the effect of selected miRNAs on trophoblast cells. Subsequently, the impact of EVs from NGT and GDM, as well as miR-515-5p, on in vivo glucose tolerance and fetal growth was assessed in pregnant mice. Results Fifty-four miRNAs showed significant differences between EVs from the adipose tissue

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.