Programming of infant neurodevelopment by maternal obesity: Potential role of maternal inflammation and insulin resistance

• Published in: Asia Pacific journal of clinical nutrition Vol. 26; no. Suppl 1; pp. S36 - S39
• Main Authors: Dewi, Mira, Carlson, Susan E, Gustafson, Kathleen M, Sullivan, Debra K, Wick, Jo A, Hull, Holly R
• Format: Journal Article
• Language: English
• Published: Clayton, Vic HEC Press 01.06.2017
• Subjects: Adult; Autism; Body Mass Index; Brain research; Central Nervous System - growth & development; Chronic illnesses; Complications; Cytokines; Cytokines - genetics; Cytokines - metabolism; Diabetes; Fasting; Female; Fetal heart rate monitoring; Gene Expression Regulation; Heart Rate; Homeostasis; Humans; Infant, Newborn; Inflammation; Inflammation - complications; Insulin resistance; Insulin Resistance - physiology; Metabolism; Nervous system; Neurodevelopmental treatment for infants; Obesity; Obesity - complications; Obesity in women; Plasma; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects - pathology; Risk factors; Studies; Systems development; Womens health
• ISSN: 0964-7058; 1440-6047
• DOI: 10.6133/apjcn.062017.s11

Background and Objectives: Recent studies show that maternal obesity is associated with impaired offspring neurodevelopmental outcomes. The mechanism underlying the association is unclear. However, there is evidence to suggest a role for intra-uterine exposure to inflammation and insulin resistance (IR). We aimed to determine if maternal IR and inflammation were associated to fetal neurodevelopment as indicated by fetal heart rate variability (HRV), an index of fetal cardiac autonomic nervous system development. Method and Study Design: A total of 44 healthy maternal-fetal pairs (maternal pre-pregnancy BMI distribution: n=20 normal weight, 8 overweight, 16 obese) were analyzed. We assessed maternal inflammation (plasma IL-6 and TNF-a) and IR (HOMA index). Fetal HRV, a proxy for fetal neurodevelopment, was assessed using fetal magnetocardiogram at the 36th week of pregnancy. The relationships between maternal inflammation and IR with fetal HRV (SD1 and SD2) were estimated individually by Pearson bivariate correlations. Results: No correlations were observed between the fetal HRV components with maternal HOMA-IR and maternal plasma levels of IL-6 and TNF-a (all p<0.05). However, the negative association between maternal TNF-a level and fetal SD2 approached significance (correlation coefficient=-0.29, 95% confidence interval=-0.62,-0.03, p=0.07). Conclusion: Maternal IR and inflammation during pregnancy were not associated with fetal cardiac autonomic nervous system development. Further studies with a larger sample size and more maternal inflammatory indicators are needed to explore these relationships.