ArticleMolecular endocrinology (Baltimore, Md.)2014
Adiponectin inhibits insulin function in primary trophoblasts by PPARα-mediated ceramide synthesis.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Maternal cardiometabolic markers are associated with fetal growth: a secondary exploratory analysis of the LIMIT randomised trial.BMC endocrine disorders · 2019Trial
- Maternal obesity results in decreased syncytiotrophoblast synthesis of palmitoleic acid, a fatty acid with anti-inflammatory and insulin-sensitizing properties.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Trial
- Role of adiponectin in gestational diabetes mellitus: advances in mechanistic insights and early predictive potential.Adipocyte · 2026Review
- Metabolic control of feto-placental development and pregnancy outcomes.Nature reviews. Endocrinology · 2026Review
- Placental mitochondrial respiration is inhibited in mice with trophoblast specific AdipoR2 overexpression.Free radical biology & medicine · 2026Article
- Obesity and Its Role in Fetal Programming-A Narrative Review.Nutrients · 2025Review
- Adipokines in preeclampsia: disrupted signaling pathways and novel therapeutic strategies.European journal of medical research · 2025Review
- Mechanisms of Fetal Overgrowth in Gestational Diabetes: The Potential Role of SOCS2.Nutrients · 2025Review
- Trophoblast-specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Regulation of placental amino acid transport in health and disease.Acta physiologica (Oxford, England) · 2024Review
- Oleic acid stimulation of amino acid uptake in primary human trophoblast cells is mediated by phosphatidic acid and mTOR signaling.FASEB bioAdvances · 2024Article
- Kinin B1 receptor controls maternal adiponectin levels and influences offspring weight gain.iScience · 2023Article
- Maternal-fetal cross-talk via the placenta: influence on offspring development and metabolism.Development (Cambridge, England) · 2023Review
- Made in the Womb: Maternal Programming of Offspring Cardiovascular Function by an Obesogenic Womb.Metabolites · 2023Review
- Review
- Normalization of maternal adiponectin in obese pregnant mice prevents programming of impaired glucose metabolism in adult offspring.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Placental Function and the Development of Fetal Overgrowth and Fetal Growth Restriction.Obstetrics and gynecology clinics of North America · 2021Review
- Placental function in maternal obesity.Clinical science (London, England : 1979) · 2020Review
- Maternal Obesity and Diabetes Mellitus as Risk Factors for Congenital Heart Disease in the Offspring.Journal of the American Heart Association · 2020Review
- Fetal Growth Trajectories and Their Association with Maternal, Cord Blood, and 5-year Child Adipokines.Journal of nutrition and metabolism · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Maternal adiponectin (ADN) levels are inversely correlated with birth weight, and ADN infusion in pregnant mice down-regulates placental nutrient transporters and decreases fetal growth. In contrast to the insulin-sensitizing effects in adipose tissue and muscle, ADN inhibits insulin signaling in the placenta. However, the molecular mechanisms involved are unknown. We hypothesized that ADN inhibits insulin signaling and insulin-stimulated amino acid transport in primary human trophoblasts by peroxisome proliferator-activated receptor-α (PPARα)-mediated ceramide synthesis. Primary human term trophoblast cells were treated with ADN and/or insulin. ADN increased the phosphorylation of p38 MAPK and PPARα. ADN inhibited insulin signaling and insulin-stimulated amino acid transport. This effect was dependent on PPARα, because activation of PPARα with an agonist (GW7647) inhibited insulin signaling and function, whereas PPARα-small interfering RNA reversed the effects of ADN on the insulin response. ADN increased ceramide synthase expression and stimulated ceramide production. C2-ceramide inhibited insulin signaling and function, whereas inhibition of ceramide synthase (with Fumonisin B1) reversed the effects of ADN on insulin signaling and amino acid transport. These findings are consistent with the model that maternal ADN limits fetal growth mediated by activation of placental PPARα and ceramide synthesis, which inhibits placental insulin signaling and amino acid transport, resulting in reduced fetal nutrient availability.
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Registered trials
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