Evidence map›Paper›PMID 40369565›Full record

ArticleCardiovascular diabetology2025

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

Nanthini Jayabalan, Soumyalekshmi Nair, Andrew Lai, Katherin Scholz-Romero, Melissa Razo-Azamar, Valeska Ormazabal, Ratana Lim, Flavio Carrion, Dominic Guanzon, Gregory E Rice and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Nanthini JayabalanTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia. n.jayabalan@uq.edu.au.
Soumyalekshmi NairTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Andrew LaiTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Katherin Scholz-RomeroTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Melissa Razo-AzamarTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Valeska OrmazabalFaculty of Biological Sciences, Pharmacology Department, University of Concepcion, Concepción, Chile.
Ratana LimObstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, VIC, Australia.
Flavio CarrionDepartamento de Investigación, Postgrado y Educación Continua (DIPEC), Facultad de Ciencias de la Salud, Universidad del Alba, Santiago, Chile.
Dominic GuanzonTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Gregory E RiceTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia.
Harold David McIntyreMater Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Martha LappasObstetrics, Nutrition and Endocrinology Group, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, VIC, Australia.
Carlos SalomonTranslational Extracellular Vesicles in Obstetrics and Gynae-Oncology Group, University of Queensland Centre for Clinical Research, Faculty of Medicine, The University of Queensland, Brisbane, QLD, 4029, Australia. c.salomongallo@uq.edu.au.

Funding

National Health and Medical Research Council 1195451
6 · The paper itself

Abstract

backgroundGestational 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.

methodsThis 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.

resultsFifty-four miRNAs showed significant differences between EVs from the adipose tissue of NGT and GDM groups. EVs from GDM increased glucose uptake in trophoblast cells, whereas EVs from NGT increased the secretion of CXCL8, IL-6, CXCL1, CXCL4, and CXCL5 from trophoblasts compared to the effect without EVs. Specifically, miR-515-5p increased glucose uptake and abolished TNF-α-dependent increase in pro-inflammatory cytokines and chemokines from trophoblast cells. Injection of pregnant mice with EVs from NGT adipose tissue loaded with miR-515-5p resulted in increased fetal weight and glucose levels.

conclusionmiR-515-5p, specifically encapsulated within EVs from omental adipose tissue in GDM, regulates placental nutrient uptake, glucose homeostasis, and fetal growth.

Indexed as

Adipose TissueBlood GlucoseDiabetes, GestationalExtracellular VesiclesFetal DevelopmentMicroRNAsPlacentaTrophoblastsAdultAnimalsCase-Control StudiesCytokinesDisease Models, AnimalFemaleGene Expression Regulation, DevelopmentalHumansBlood GlucoseCytokinesInflammation MediatorsMicroRNAsAdipose tissueExtracellular vesiclesFetal growthGestational diabetesGlucose uptakePlacenta

Identifiers

PMID40369565
PMCPMC12080180

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.