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Patel, Nashita; Hellmuth, Christian; Uhl, Olaf; Godfrey, Keith; Briley, Annette; Welsh, Paul; Pasupathy, Dharmintra; Seed, Paul T.; Koletzko, Berthold und Poston, Lucilla (2018): Cord Metabolic Profiles in Obese Pregnant Women: Insights Into Offspring Growth and Body Composition. In: Journal of Clinical Endocrinology & Metabolism, Bd. 103, Nr. 1: S. 346-355

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Abstract

Context: Offspring exposed in utero to maternal obesity have an increased risk of later obesity;however, the underlying mechanisms remain unknown. Objective: To assess the effect of an antenatal lifestyle intervention in obese women on the offspring's cord blood metabolic profile and to examine associations of the cord blood metabolic profile with maternal clinical characteristics and offspring anthropometry at birth and age 6 months. Design: Randomized controlled trial and cohort study. Setting: The UK Pregnancies Better Eating and Activity Trial. Participants: Three hundred forty-four mother-offspring pairs. Intervention: Antenatal behavioral lifestyle (diet and physical activity) intervention. Main Outcome Measures: Targeted cord blood metabolic profile, including candidate hormone and metabolomic analyses. Results: The lifestyle intervention was not associated with change in the cord blood metabolic profile. Higher maternal glycemia, specifically fasting glucose at 28 weeks gestation, had a linear association with higher cord blood concentrations of lysophosphatidylcholines (LPCs) 16.1 (beta = 0.65;95% confidence interval: 0.03 to 0.10) and 18.1 (0.52;0.02 to 0.80), independent of the lifestyle intervention. A principal component of cord blood phosphatidylcholines and LPCs was associated with infant z scores of birth weight (0.04;0.02 to 0.07) and weight at age 6 months (0.05;0.00 to 0.10). Cord blood insulin growth factor (IGF)-1 and adiponectin concentrations were positively associated with infant weight z score at birth and at 6 months. Conclusions: Concentrations of LPCs and IGF-1 in cord blood are related to infant weight. These findings support the hypothesis that susceptibility to childhood obesity may be programmed in utero, but further investigation is required to establish whether these associations are causally related.

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