ReviewWorld journal of hepatology2025
Liver as a metabolic sensor in gestational diabetes: Implications for offspring's liver and diabetes risk.
Review in World journal of hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- FGF21 and SHBG as Putative Hepatic Axes in Maternal Metabolic Adaptation: A Hypothetical Framework for Postpartum Insulin Sensitivity Restoration.Biomolecules · 2026Review
- Mechanisms of postpartum metabolic dysfunction-associated steatotic liver disease in women with a history of gestational diabetes mellitus.Endocrine connections · 2026Review
- Early-pregnancy trunk phase angle derived from bioelectrical impedance analysis for the prediction of gestational diabetes mellitus.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gestational diabetes mellitus (GDM) is increasingly recognized not only for its immediate obstetric complications but also for its long-term metabolic consequences in both mothers and their offspring. Traditionally, research has emphasized the roles of pancreatic β-cell dysfunction and placental dysregulation in GDM. However, emerging evidence highlights the maternal liver as a central metabolic hub during pregnancy coordinating glucose, lipid, and hormonal adaptations essential for fetal development. This review synthesizes current findings on how GDM disrupts the maternal liver's adaptive roles, transforming it from a metabolic coordinator into a source of maladaptive endocrine, inflammatory, and nutrient signals. It outlines key mechanistic pathways through which maternal hepatic dysfunction may increase offspring susceptibility to non-alcoholic fatty liver disease and type 2 diabetes mellitus. These include hepatokine dysregulation, altered lipid metabolism, impaired insulin signaling, inflammatory and oxidative stress pathways, and epigenetic and transcriptomic reprogramming. In addition, it explores novel axes such as the gut-liver-placenta interplay, bile acid signaling disruptions, endoplasmic reticulum stress responses, and extracellular vesicle-mediated communication. By reframing the maternal liver's role in GDM pathophysiology, this review identifies critical windows for early clinical intervention and highlights the potential for liver-focused strategies to prevent the intergenerational transmission of metabolic disease.
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