ArticleFrontiers in cell and developmental biology2024
Vitamin E supplementation prevents obesogenic diet-induced developmental abnormalities in SR-B1 deficient embryos.
Article in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Dietary Interventions Targeting Maternal Obesity: Intergenerational Effects, Mechanisms, and Translational Insights.Current nutrition reports · 2026Review
- Lipid Remodeling in Mouse SR-B1-Deficient Embryos with Oxidative Stress-Associated Neural Tube Defects.Antioxidants (Basel, Switzerland) · 2026Article
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5 authors.
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Abstract
Introduction: Genetic and environmental factors influence the risk of neural tube defects (NTD), congenital malformations characterized by abnormal brain and spine formation. Mouse embryos deficient in Scavenger Receptor Class B Type 1 (SR-B1), which is involved in the bidirectional transfer of lipids between lipoproteins and cells, exhibit a high prevalence of exencephaly, preventable by maternal vitamin E supplementation. SR-B1 knock-out (KO) embryos are severely deficient in vitamin E and show elevated reactive oxygen species levels during neurulation. Methods: We fed SR-B1 heterozygous female mice a high-fat/high-sugar (HFHS) diet and evaluated the vitamin E and oxidative status in dams and embryos from heterozygous intercrosses. We also determined the incidence of NTD. Results and discussion: HFHS-fed SR-B1 HET females exhibited altered glucose metabolism and excess circulating lipids, along with a higher incidence of embryos with developmental delay and NTD. Vitamin E supplementation partially mitigated HFHS-induced maternal metabolic abnormalities and completely prevented embryonic malformations, likely through indirect mechanisms involving the reduction of oxidative stress and improved lipid handling by the parietal yolk sac.
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