Evidence mapPaperPMID 40186686Full record

ArticleDiabetologia2025

Cardiac remodelling, recognition memory deficits and accelerated ageing in a rat model of gestational diabetes.

Sathya Velmurugan, Vivek K Pandey, Nirmal Verma, Deepak Kotiya, Florin Despa, Sanda Despa

Abstract read
In one paragraph

Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
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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

6 authors.

Sathya Velmurugan *Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0003-0769-8424
Vivek K Pandey *Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0003-4612-6138
Nirmal VermaDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0002-9218-2475
Deepak KotiyaDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0001-5794-8626
Florin DespaDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA.ORCID http://orcid.org/0000-0002-5879-6449
Sanda DespaDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA. s.despa@uky.edu.ORCID http://orcid.org/0000-0002-2374-6177

Funding

American Heart Association 19TPA34850094NHLBI NIH HHS HL148443NHLBI NIH HHS R01 HL135000NHLBI NIH HHS R01 HL148443NIA NIH HHS AG057290NIA NIH HHS R01 AG057290NINDS NIH HHS NS116058NINDS NIH HHS R01 NS116058
6 · The paper itself

Abstract

aims/hypothesisWomen with prior gestational diabetes mellitus (GDM) have higher incidence of age-associated diseases, including type 2 diabetes, CVD and cognitive impairment. Human studies cannot readily determine whether GDM causes these conditions or the underlying mechanisms. Here we used a well-validated rat model of GDM to address these questions.

methodsRats with beta cell-specific expression of human amylin, a pancreatic hormone, were used as a GDM model. Five-month-old female rats were randomly assigned to no-pregnancy, one-pregnancy and two-pregnancies experimental groups. GTTs and transthoracic echocardiography were performed at baseline and during the postpartum period. At 18 months of age, the novel object recognition test was administered, followed by euthanasia and organ collection.

resultsAll female rats developed glucose intolerance and showed cardiac remodelling and impaired left ventricular relaxation with ageing. Glucose intolerance was exacerbated in rats with prior GDM pregnancies compared with nulliparous rats, with significant differences starting at 9 months of age. However, blood glucose levels were comparable in the three groups during the course of the study. Rats with two GDM-complicated pregnancies had increased left ventricular mass compared with the other groups following the second pregnancy and until the end of the study. At 18 months of age, rats with prior GDM pregnancies presented aggravated demyelination, particularly in the hippocampus and mid-brain region, oxidative stress and neuroinflammation, and had a lower recognition index in the novel object recognition test compared with nulliparous rats. Higher parity exacerbated these effects. Shorter telomeres and reduced mitochondrial DNA content, two hallmarks of biological ageing, were found in the brain, heart and pancreas of rats with prior GDM. CONCLUSIONS/

interpretationThese findings support the concept that GDM is a sex-specific risk factor for ageing-related diseases, and point to accelerated cellular ageing as a contributing mechanism. DATA AVAILABILITY: Cardiac echocardiography and GTT data are available at Dataverse under the identifier https://doi.org/10.7910/DVN/R2HITG.

Indexed as

AgingDiabetes, GestationalMemory DisordersVentricular RemodelingAnimalsBlood GlucoseDisease Models, AnimalFemaleGlucose IntolerancePregnancyRatsBlood GlucoseCardiac hypertrophyCellular ageingCognitive impairmentGestational diabetes

Identifiers

PMID40186686
PMCPMC12305478

What Socratic holds

Textmetadata
LicenceTDM
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Registered trials

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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 Socratic graph.