ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2015
Glucose and metformin modulate human first trimester trophoblast function: a model and potential therapy for diabetes-associated uteroplacental insufficiency.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 74 citations in OpenAlex.
- Predictive Value for Preeclampsia of sFlt-1:PlGF Ratio in Pregnancy Complicated by Gestational Diabetes.Diabetes/metabolism research and reviews · 2026Observational
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- The Impact of Maternal Obesity and Diabetes on the Development of Congenital Heart Defects (CHDs) in Offspring: A Narrative Review.Metabolites · 2026Review
- Metabolic, microbial, and pharmacological stimuli elicit distinct lipidomic and cytokine responses in the human placenta.Molecular human reproduction · 2026Article
- Article
- Is Gestational Diabetes Mellitus Associated with Peripartum Infections?Microorganisms · 2025Article
- Article
- Modified lipoprotein-induced sFlt1 production in human placental trophoblasts is mediated by protein kinase C.European journal of pharmacology · 2025Article
- Hyperglycemia enhances group BFrontiers in immunology · 2025Article
- Evaluating oxidative stress targeting treatments inFrontiers in cell and developmental biology · 2025Article
- Sirtuins and Their Implications in the Physiopathology of Gestational Diabetes Mellitus.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Gestational Diabetes Mellitus-Induced Inflammation in the Placenta via IL-1β and Toll-like Receptor Pathways.International journal of molecular sciences · 2024Article
- Physical Activity as a Modern Intervention in the Fight against Obesity-Related Inflammation in Type 2 Diabetes Mellitus and Gestational Diabetes.Antioxidants (Basel, Switzerland) · 2023Review
- Review
- High Glucose Promotes Inflammation and Weakens Placental Defenses againstInternational journal of molecular sciences · 2023Article
- Associations Between Preconception Glycemia and Preterm Birth: The Potential Role of Health Care Access and Utilization.Journal of women's health (2002) · 2023Article
- Pathophysiological impact of CXC and CX3CL1 chemokines in preeclampsia and gestational diabetes mellitus.Frontiers in cell and developmental biology · 2023Review
- Hyperglycemia disturbs trophoblast functions and subsequently leads to failure of uterine spiral artery remodeling.Frontiers in endocrinology · 2023Review
- Gut Microbiome Changes in Gestational Diabetes.International journal of molecular sciences · 2022Review
- Maternal Exposure to Fine Particulate Matter and Its Chemical Components Increasing the Occurrence of Gestational Diabetes Mellitus in Pregnant Japanese Women.JMA journal · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
problemDiabetes confers an increased risk of preeclampsia, but its pathogenic role in preeclampsia is poorly understood. The objective of this study was to elucidate the effects of excess glucose on trophoblast function and whether any changes could be reversed by metformin. METHOD OF STUDY: The human first trimester trophoblast cell line (Sw.71) was treated with glucose at 5, 10, 25, and 50 mm, in the presence and absence of metformin. Trophoblast migration was quantified and supernatant cytokine, chemokine, and angiogenic factors measured.
resultsIncreasing concentrations of glucose significantly increased trophoblast secretion of the inflammatory cytokines/chemokines: IL-1β, IL-6, IL-8, GRO-α, RANTES, and G-CSF; significantly increased trophoblast secretion of the anti-angiogenic factors sFlt-1 and sEndoglin; and significantly decreased trophoblast migration. Excess glucose-induced trophoblast IL-1β production was inhibited by disabling the Nalp3/ASC inflammasome. Metformin partially reduced the glucose-induced inflammatory response, but had no effect on the anti-angiogenic or antimigratory response.
conclusionExcess glucose induced a pro-inflammatory, anti-angiogenic, and antimigratory state in first trimester trophoblast cells. Glucose-induced trophoblast IL-1β secretion was mediated by the inflammasome. Glucose-induced inflammation was partially reversed by metformin. These findings demonstrate the pleiotropic effects of hyperglycaemia on the trophoblast, providing potential explanations for the strong link between diabetes and preeclampsia.
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