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Background Offspring of obese rodents develop a metabolic phenotype that favors fat deposition. Data regarding the impact of maternal obesity programing of offspring fuel usage in humans is scarce. Objective The objective of this study was to explore the association between maternal weight status and dietary palmitate oxidation (DPO) in 2-y-old offspring, taking into consideration potential confounders and modifiers. Methods Women (n  = 56) were enrolled by the first trimester of gestation. Maternal physical activity (PA; measured with accelerometers) at enrollment and gestational weight gain (GWG) were measured. Offspring sex, race, and breastfeeding (BF) duration were self-reported. Human milk (HM) composition was determined at 6 mo postpartum. At age 2 y, dietary quality [healthy eating index (HEI)] and parental feeding practices [Child Feeding Questionnaire (CFQ)] were assessed. DPO in 2-y-olds (2-yo-DPO) was measured using deuterated palmitic acid. Generalized linear regression analysis was used to model the associations of 2-yo-DPO with maternal weight status [normal weight (NW), BMI <25 (in kg/m2) compared with excessive weight (EW), BMI ≥25]. Results DPO was higher in offspring of women with EW compared with NW (2.1 ± 1.2%/h compared with 1.4 ± 0.7%/h, P  = 0.03). Maternal weight status interacted with BF duration in association with 2-yo-DPO (log ß : 0.05, P  = 0.04). Specifically, 2-yo-DPO was higher in the EW compared with NW group if BF duration was ≥9 mo. HM insulin (log ß : 0.35, P  = 0.002) and HM leptin (log ß : 0.81, P  = 0.001) concentrations directly associated with 2-yo-DPO. PA (log ß : 0.06, P  = 0.013), parental feeding restriction (log ß : 0.05, P  < 0.0001), and male sex (log ß : 0.54, P  < 0.001) were positively associated with 2-yo-DPO. HEI was negatively associated with 2-yo-DPO (log ß :−0.03, P  < 0.0001). Conclusions Higher 2-yo-DPO in offspring of women with EW compared with NW were driven by BF duration. Higher HM insulin and leptin concentrations in women with EW may explain these finding. More studies are needed to confirm these results. This trial was registered at clinicaltrials.gov as NCT03281850. [ABSTRACT FROM AUTHOR]

Background Human milk composition is altered by maternal obesity. The association between milk metabolites and infant outcomes has not been thoroughly investigated. Objectives This study aimed to quantify maternal adiposity-related differences in the human milk metabolome and to identify metabolites associated with infant adiposity during the first 6 mo postpartum using untargeted metabolomics. Method Maternal anthropometrics were assessed ≤14 weeks of gestation. Human milk samples were collected at 0.5 mo (n  = 159), 2 mo (n  = 131), and 6 mo (n  = 94) postpartum from normal weight (NW, BMI = 18.5–24.9 kg/m2) and obese (OB, BMI >30 kg/m2) mothers. GC-time-of-flight-MS was used to identify metabolic signatures that discriminate NW and OB women. Partial least squared (PLS)-discriminant analysis, and PLS-regression models were assessed to examine relations between metabolites and maternal BMI and fat mass. Metabolites altered by maternal obesity were used in linear mixed effect models to predict infant adiposity. Results Multivariate modeling identified 23, 17, and 10 metabolites that described maternal adiposity indices at 0.5 mo, 2 mo, and 6 mo postpartum, respectively. Monosaccharides and sugar alcohols were the most representative annotated metabolite classes that were increased in milk from OB women and included: mannose, ribose, lyxose, lyxitol (0.5 mo); mannose, ribitol, glycerol, isothreonic acid, lyxitol (2 mo); lyxitol and isothreonic acid (6 mo). Other discriminant metabolites included: 1-monostearin, xylonolactone, shikimic acid, pseudo uridine, and dodecanol (0.5 mo); N -acetyl-D-hexosamine and fumaric acid (2 mo); uric acid and tyrosine (6 mo). Mannose, lyxitol, and shikimic acid predicted higher infant adiposity over the first 6 mo of life. Conclusions This study reports on 1 of the largest cohorts to date examining the metabolic profiles in human milk comparing NW and OB women. Maternal adiposity was associated with increased amounts of milk nonglucose monosaccharides. Human milk metabolomics may be useful in predicting infant adiposity. These trials were registered at www.clinicaltrials.gov as NCT01131117 and NCT02125149. [ABSTRACT FROM AUTHOR]

Background Studies indicate that maternal weight status modulates human milk composition; however, results are conflicting. Objectives Our objective was to examine the relation between maternal body composition and human milk macronutrients and bioactive components and also their association with infant daily intakes and body composition. Methods Human milk samples were obtained from a longitudinal study (NCT 01131117) in normal weight (NW: 18.5–24.9 kg/m2, n  = 88) and overweight/obese (OW: 25–35 kg/m2, n  = 86) women between 0.5 and 9 mo postpartum. Macronutrient content was estimated using mid-infrared spectroscopy. Leptin, insulin, and C-reactive protein (CRP) were measured using electrochemiluminescence immunoassays. Infant body composition was obtained using quantitative MRI. Linear mixed models were adjusted for postpartum age and infant sex. Results Human milk in OW mothers was higher in fat and protein and lower in carbohydrate content at some time points compared with that in NW mothers. Human milk leptin, insulin, and CRP concentrations were higher in OW mothers compared with NW mothers, with infants of OW mothers exposed to 1.5–2.5 times higher concentrations of leptin and insulin compared with infants of NW mothers. Similar results were observed when concentrations were normalized to infant daily intake and body weight. The effect sizes of infant daily intakes associated with infant growth parameters were small for macronutrients [0.005–0.05 z -score units and 0.02–0.45 fat mass index (FMI) or fat-free mass index units per unit of change in composition, P  < 0.05]. Larger effect sizes were seen with human milk insulin and leptin (0.24 z -score units and 0.37–1.15 FMI units per unit of change in composition, P  < 0.05). Conclusions These findings demonstrate that infants of OW mothers are exposed to higher concentrations of insulin, leptin, and, to a lesser extent, CRP. The bioavailability of these 3 human milk bioactives and their mechanisms of action in the infant are unclear. This trial was registered at clinicaltrials.gov as NCT01131117. [ABSTRACT FROM AUTHOR]

Summary: Background: Maternal obesity increases offspring's obesity risk. However, studies have not often considered maternal metabolic and exercise patterns as well as paternal adiposity as potential covariates. Objective: To assess the relationship between parental and newborn adiposity. Methods: Participants were mother‐child pairs (n = 209) and mother‐father‐offspring triads (n = 136). Parental (during gestation) and offspring (2 weeks old) percent fat mass (FM) were obtained using air displacement plethysmography. Maternal race, age, resting energy expenditure (indirect calorimetry), physical activity (accelerometry), gestational weight gain (GWG), gestational age (GA), delivery mode, infant's sex and infant feeding method were incorporated in multiple linear regression analyses. The association between parental FM and offspring insulin‐like growth factor 1 (IGF‐1) was assessed at age 2 years. Results: Maternal adiposity was positively‐associated with male (β = 0.11, P =.015) and female (β = 0.13, P =.008) infant FM, whereas paternal adiposity was negatively‐associated with male newborn adiposity (β = ‐0.09, P =.014). Breastfeeding, female sex, GA and GWG positively associated with newborn adiposity. Vaginal and C‐section delivery methods associated with greater adiposity than vaginal induced delivery method. Plasma IGF‐1 of 2‐year‐old boys and girls positively associated with their respective fathers' and mothers' FM. Conclusions: Maternal and paternal adiposity differentially associate with newborn adiposity. The mechanisms of this finding remain to be determined. [ABSTRACT FROM AUTHOR]

Human milk oligosaccharides (HMOs) are bioactive molecules playing a critical role in infant health. We aimed to quantify the composition of HMOs of women with normal weight (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), or obesity (30.0–60.0 kg/m2) and determine the effect of HMO intake on infant growth. Human milk (HM) samples collected at 2 months (2 M; n = 194) postpartum were analyzed for HMO concentrations via high-performance liquid chromatography. Infant HM intake, anthropometrics and body composition were assessed at 2 M and 6 M postpartum. Linear regressions and linear mixed-effects models were conducted examining the relationships between maternal BMI and HMO composition and HMO intake and infant growth over the first 6 M, respectively. Maternal obesity was associated with lower concentrations of several fucosylated and sialylated HMOs and infants born to women with obesity had lower intakes of these HMOs. Maternal BMI was positively associated with lacto-N-neotetraose, 3-fucosyllactose, 3-sialyllactose and 6-sialyllactose and negatively associated with disialyllacto-N-tetraose, disialyllacto-N-hexaose, fucodisialyllacto-N-hexaose and total acidic HMOs concentrations at 2 M. Infant intakes of 3-fucosyllactose, 3-sialyllactose, 6-sialyllactose, disialyllacto-N-tetraose, disialyllacto-N-hexaose, and total acidic HMOs were positively associated with infant growth over the first 6 M of life. Maternal obesity is associated with changes in HMO concentrations that are associated with infant adiposity. [ABSTRACT FROM AUTHOR]