Observational studyFrontiers in endocrinology2026
Gestational diabetes mellitus-induced adipokine dysregulation and links to metabolic programming risks.
Observational study in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Redox Biomarker Alterations and Disrupted Uric Acid-Catalase Activity Association in Gestational Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Gestational diabetes mellitus (GDM) is a pregnancy-related hyperglycemic disorder with highly variable global prevalence, largely driven by differences in diagnostic criteria, maternal characteristics, and lifestyle factors, which complicates efforts to standardize screening and prevention. GDM disrupts maternal-fetal glucose homeostasis, leading to fetal exposure to hyperglycemia and hyperinsulinemia, and is associated not only with immediate obstetric complications but also with long-term metabolic risk in both mothers and offspring. Objective: This study evaluated the impact of maternal hyperglycemia, classified as diet-controlled (GDM-diet) or insulin-treated (GDM-insulin), on leptin, adiponectin, soluble leptin receptor (sLeptinR), and the derived indices leptin-to-adiponectin ratio (LAR) and free leptin index (FLI) across the maternal-fetal axis. Design: This study was a retrospective observational cohort study targeting patients with gestational diabetes mellitus. Maternal and cord blood plasma from 30 hyperglycemic and 23 normoglycemic mothers were analyzed for leptin, adiponectin, and soluble leptin receptor concentrations using immunoenzymatic assays. Results: Maternal plasma leptin concentrations were significantly higher in the GDM-insulin group (10.05 ng/mL) than in non-GDM pregnancies (4.44 ng/mL; Conclusion: These findings point to leptin, adiponectin, FLI, and LAR as possible metabolic indicators of GDM-linked insulin resistance, and low-grade inflammation. Higher maternal leptin, LAR, and FLI, alongside stable sLeptinR, signal leptin resistance, which disrupts placental nutrient transport and links maternal metabolic stress to fetal anthropometric measures. Tracking these markers could guide postnatal steps to cut long-term metabolic risks across the next generations.
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Registered trials
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