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Background: Maternal nutritional status affects placental function, which may underlie the intrauterine origins of obesity and diabetes. The extent to which diet quality is associated with placental signaling and which specific pathways are impacted is unknown.Objectives: To examine sex-specific associations of maternal diet quality according to the Healthy Eating Index (HEI)-developed to align with recommendations from the Dietary Guidelines for Americans-with placental proteins involved in metabolism and mediators of environmental stress, inflammation, and growth factors.Methods: Among 108 women from the Healthy Start cohort with a mean ± SD age of 29.0 ± 6.1 y and a prepregnancy BMI (in kg/m2) of 24.8 ± 5.3, we conducted multivariable linear regression analysis stratified by offspring sex. We adjusted for maternal race or ethnicity, age, education, prenatal smoking habits, and physical activity and tested for an association of maternal HEI >57 compared with ≤57 and the abundance and phosphorylation of key proteins involved in insulin/growth factor signaling; mediators of environmental stress, inflammation, and growth factors; mechanistic target of rapamycin signaling proteins; and energy sensing in placental villus samples. HEI >57 was chosen given its prior relevance among Healthy Start mother-child dyads.Results: In adjusted models, HEI >57 was associated with greater abundance of insulin receptor β (0.80; 95% CI: 0.11, 1.49) in placentas of females. In males, maternal HEI >57 was associated with greater activation and abundance of select placental nutrient-sensing proteins and environmental stress, inflammation, and growth factor proteins (S6K1Thr389/S6K1: 0.81; 95% CI: 0.21, 1.41; JNK1Thr183/Tyr185/JNK1: 0.82; 95% CI: 0.27, 1.37; JNK2Thr183/Tyr185/JNK2: 0.57; 95% CI: 0.02, 1.11).Conclusions: Higher-quality diet had sex-specific associations with placental protein abundance/phosphorylation. Given that these proteins have been correlated with neonatal anthropometry, our findings provide insight into modifiable factors and placental pathways that should be examined in future studies as potential links between maternal diet and offspring metabolic health. This trial was registered at clinicaltrials.gov as NCT02273297. [ABSTRACT FROM AUTHOR]

Background: Pregnancies complicated by maternal obesity are characterized by metabolic differences affecting placental nutrient transport and fetal development. Docosahexaenoic acid (DHA) is critical for fetal brain development and is primarily incorporated into phosphatidylcholine (PC). Recent evidence suggests that choline may enhance PC-DHA synthesis; however, data on the impact of maternal plasma choline on placental phospholipid DHA content in females with obesity are limited., Methods: We conducted a secondary analysis of a DHA supplementation trial (800 mg/d) in 38 pregnant females with obesity (body mass index ≥30 kg/m 2 ). Blood samples at 36 wk gestation and term placentas were analyzed for phospholipids using mass spectrometry. Choline transporter-like (CTL) proteins in the syncytiotrophoblast microvillous (MVM) and basal plasma membranes were quantified by Western blot., Results: Daily DHA supplementation from 25 wk gestation was associated with higher maternal plasma and placental PC- and lysophosphatidylcholine (LPC)-DHA. A significant interaction (P interaction <0.05) between DHA supplementation and choline indicated that higher choline enhanced the incorporation of DHA into plasma PC. MVM CTL-1 expression was correlated with placental total PC-DHA and LPC-DHA content, suggesting that CTL-1 has a predominate role in placental choline uptake and phospholipid synthesis., Conclusions: These findings suggest that choline may influence maternal PC- and LPC-DHA synthesis and plasma levels, as well as the expression of placental choline transporters and the resulting PC- and LPC-DHA content in females with obesity. These relationships may have implications for DHA transport to the fetus and overall fetal development., Competing Interests: Conflict of interest The authors report no conflicts of interest., (Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)