Association between maternal obesity and neonatal folate and vitamin B12 status: Functional biomarkers and placental transporters.

Pregestational obesity increases the risk of vitamin deficiencies in mothers, yet its impact on neonatal status and placental transporters is unclear. This study investigates the association between pregestational obesity and neonatal folate and vitamin B12 levels, as well as their biomarkers and the expression of placental transporters. This cross-sectional study included women with pregestational overweight or obesity (Body mass index [BMI]>25 kg/m²; Overweight/Obesity [Ob] group) and healthy weight (BMI<25 kg/m²; healthy weight [HW] group). In mothers and newborns, folate status was measured in plasma and red blood cells using liquid chromatography-tandem mass spectrometry to identify six chemical forms, and total vitamin B12 was quantified by electrochemiluminescence immunoassay, holotranscobalamin by chemiluminescent microparticle immunoassay, methylmalonic acid by liquid chromatography-tandem mass spectrometry, and total homocysteine by high-performance liquid chromatography with fluorescence detector in plasma. Placental folate receptor alpha (FOLR1) and transcobalamin receptor (TCblR/CD320) were determind using RT-qPCR reaction and Western blot. A P value <.05 was considered statistically significant. Women in the Ob-group had lower red blood cell folate status than those in the HW-group. Newborns of Ob-groups had decreased folate forms, total vitamin B12, holotranscobalamin, and higher methylmalonic acid. Female newborns of the Ob-group exhibites greater folate and vitamin B12 depletion than females in the HW. Placental expression of FOLR1 (protein) and TCblR/CD320 (mRNA) was lower in the Ob-group. Conversely, FOLR1 and TCblR/CD320 (mRNA and protein) were higher in female compared to male placentas (P<.05). Maternal obesity is associated with decreased neonatal folate and vitamin B12 levels, as confirmed by functional biomarkers. Altered placental FOLR1 and CD320 expression suggests impaired vitamin transport in obesity. The sex-specific differences may indicate an adaptive response in the female placenta, but further studies of mechanisms are warranted.