TY - JOUR
T1 - Vitamin E supplementation prevents obesogenic diet-induced developmental abnormalities in SR-B1 deficient embryos
AU - Quiroz, Alonso
AU - Belledonne, Gabriela
AU - Saavedra, Fujiko
AU - González, Javier
AU - Busso, Dolores
N1 - Publisher Copyright:
Copyright © 2024 Quiroz, Belledonne, Saavedra, González and Busso.
PY - 2024
Y1 - 2024
N2 - 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.
AB - 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.
KW - embryo development
KW - malnutrition by excess
KW - neural tube defects
KW - SR-B1 deficiency
KW - vitamin E
UR - http://www.scopus.com/inward/record.url?scp=85207431209&partnerID=8YFLogxK
UR - http://www.ncbi.nlm.nih.gov/pubmed/39445334
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC11496146
UR - https://www.mendeley.com/catalogue/6f959d7d-b051-3740-8366-76c267d9938e/
U2 - 10.3389/fcell.2024.1460697
DO - 10.3389/fcell.2024.1460697
M3 - Article
C2 - 39445334
AN - SCOPUS:85207431209
SN - 2296-634X
VL - 12
SP - 1460697
JO - Frontiers in Cell and Developmental Biology
JF - Frontiers in Cell and Developmental Biology
M1 - 1460697
ER -