196-LB: Prenatal and Lifestyle Contributions to Child Insulin Sensitivity

Abstract

Background: Early life exposures play an important role in metabolic health throughout life. We examined how prenatal exposures to maternal obesity or gestational diabetes mellitus (GDM) and low levels of physical activity and increased food intake may contribute to reductions in insulin sensitivity in childhood. Methods: Participants were 7-10 year old children who were born at Kaiser Permanente Southern California. Maternal pre-pregnancy BMI and GDM status were extracted from electronic medical records. Child weight and height were measured, and oral glucose tolerance tests were performed. Insulin sensitivity was estimated using the Matsuda insulin sensitivity index (ISI). Diet was assessed using 24-hour dietary recalls and daily energy intake (EI) was calculated. Physical activity was assessed using a 3-day physical activity recall and average min/day of moderate to vigorous physical activity (MVPA) was calculated. Linear regression was used to assess ISI associations with the exposures. Results: 92 children (52 girls; 40 boys; 55 GDM-exposed; 37 unexposed) participated. Maternal pre-pregnancy BMI ranged from 19.0-50.4 kg/m2. Mean±SD child age was 8.3±0.9 years, BMI z-score: 0.60±1.1, ISI: 10.6±5.9, EI: 1790.7±444.2 kcal, and MVPA: 118.7±93.8 min/day. Children who spent more time in MVPA had better insulin sensitivity (β=0.82; P=.02). Adjusting for maternal pre-pregnancy BMI, GDM exposure, child age, sex, and EI, did not affect this relationship (β=0.87; P<.01), nor did further adjusting for BMI z-score (β=0.78; P=.01). Prenatal exposure to GDM and child ISI (β=0.19, P=.28) and maternal pre-pregnancy BMI were not significantly associated with child ISI (β=-0.01, P=0.40), nor was child’s EI associated with ISI (β=0.001; P=.59). Conclusions: Time spent in MVPA was the strongest predictor of child insulin sensitivity. Our findings suggest that engaging in MVPA during childhood is beneficial for insulin sensitivity and may help ameliorate future risk for metabolic disease. Disclosure J. Alves: None. T. Chow: None. J. Zink: None. S. Luo: None. M.P. Martinez: None. A. Romero: None. A. Xiang: None. K.A. Page: None. Funding American Diabetes Association (1-14-ACE-36 to K.A.P.); National Institutes of Health (1F31MH115640-01A1)