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Life sciences · Journal article
Lipids in Health and Disease · September 2, 2026
Early or partial results. Treat as a signal, not a conclusion.
This cross-sectional observational study reports associations between altered placental sphingolipid content (particularly decreased ceramides and sphingomyelins) and maternal obesity, GDM, and birthweight z-score. The findings are correlational and mechanistic in nature, raising a hypothesis about sphingolipid-mediated regulation of fetal growth but providing no evidence of causation or clinical intervention.
Cross-sectional observational study. Women at term delivery: control, obese (BMI not specified), and obese with gestational diabetes mellitus; fetal sex noted as a variable. Compared with: Control vs. obese vs. obese with GDM.
Placental ceramides decreased with maternal obesity with and without GDM, particularly in basal membrane, and were negatively correlated with birthweight and maternal BMI Ceramide synthase (CerS) expression was decreased while ceramidase (ASAH1) expression was increased and positively correlated with birthweight Sphingomyelins were specifically decreased in microvillous membrane of female placentas and negatively correlated with birthweight
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These findings are not yet actionable for clinical practice. They suggest a potential mechanism linking maternal metabolic disease to fetal overgrowth via placental sphingolipid dysregulation, but require confirmatory studies and mechanistic work before any therapeutic target can be proposed.
Observational study of placental lipid composition in a cross-sectional design with correlational analysis; no causal mechanism established and no intervention or clinical outcome tested.
As stated by the source record.
Quoted from the source exactly as published.
These findings are not yet actionable for clinical practice. They suggest a potential mechanism linking maternal metabolic disease to fetal overgrowth via placental sphingolipid dysregulation, but require confirmatory studies and mechanistic work before any therapeutic target can be proposed.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Maternal obesity and GDM increase the risk of fetal overgrowth. It has been shown that maternal adiponectin, decreased with these pregnancy pathologies, stimulates ceramide synthesis regulating placental nutrient transfer and fetal growth. We hypothesized that placental sphingolipid content, particularly ceramides, would be associated with fetal overgrowth in maternal obesity and GDM. Human term placentas from control, obese and obese with GDM women were collected. Lipidomic analysis by LC–MS/MS was performed on placental homogenates and membranes to assess sphingolipid content. Placental expression of enzymes involved in sphingolipid metabolism was studied by immunoblot. One or two-way ANOVA were used to analyze statistical differences on sphingolipid content and sphingolipid-related protein expression between groups and correlation with maternal BMI and z-score were determined with Pearson’s correlation coefficient. Placental ceramides decreased with maternal obesity with and without GDM, particularly in the basal membrane (BM), and were negatively correlated with birthweight and maternal BMI. Expression of ceramide synthase, CerS, was decreased and the expression of ceramidase, ASAH1, increased and positively correlated with birthweight. Sphingolipids such as sphingomyelins (SM) were specifically decreased in the microvillous membrane (MVM) of female placentas and negatively correlated with birthweight. The expression of sphingomyelinase (nSMase) was also positively correlated with maternal BMI and birthweight. Our results suggest a role for sphingolipids, particularly ceramides, in placental membranes in regulating fetal growth in pregnancies complicated by maternal metabolic disease and highlight the importance of fetal sex in establishing placental sphingolipid content in pregnancy pathologies.
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