Mother's Pre-Pregnancy BMI is an Important Determinant of Childhood Obesity and Adverse Cardiometabolic Outcomes

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 677-696-Obesity Physiology & Epidemiology
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-686
Hong Chang Tan*1, James M Roberts2, Janet M Catov3 and Fida F Bacha1
1Children's Nutrition Research Center, Houston, TX, 2Magee Women's Research Institute, Pittsburgh, PA, 3Magee Women's Research Institute, Pittsburg, PA
Familial aggregation of body mass indices (BMI) is well established. More recent evidence linked maternal obesity with the risk of childhood obesity, insulin resistance, and type 2 diabetes. This study aimed to evaluate the effects of maternal pre-pregnancy BMI on the cardiometabolic profile of the offspring.

Fifty-two children born to mothers with a pre-pregnancy BMI ≥25 kg/m2 (OW group, n=27) or  BMI <25 kg/m2 (NW group, n=25) were studied. The children were recruited (1:1) to be from either uncomplicated gestation or a gestation complicated by preeclampsia or chronic hypertension. Birth records, demographic, and anthropometric measurements were obtained. A subset of children (n=45) underwent fasting blood samples for HbA1C, fasting lipids, CRP, body composition using DXA and oral glucose tolerance test. Results were reported as mean ± SD.

There were no significant differences in gestational comorbidities between the OW and NW groups (40.7 vs 44%). Gestational age (GA) (38.1±3.1 vs 36.8±7.4 weeks) and birth weight (BW) percentile for GA (43.4±33.4 vs 49.7±29.1) were similar. Children born to OW mothers were similar in age (13.4±2.7 vs 12.7±3.3 years), gender, ethnicity and Tanner stage at study evaluation. However, they had a significantly higher age and sex adjusted BMI % (81.1±25.7 vs 60.3±26.4, p<0.01) and % body fat (32.4±9.0 vs 25.2±5.7, p<0.01). This translated to a 6-fold greater risk to be obese/overweight (66.7% vs 24 %; OR 6.3, p<0.01). They also had higher systolic BP (111.7±10.9 vs 105.6±9.2, p=0.04), lower HDL (46.6 ± 9.4 vs 54.9± 8.6 md/dL, p<0.01), higher TG (87.1±39.9 vs 59.7±24.9 md/dL, p<0.01), and higher CRP (2.0 ± 2.4 vs 0.4±0.3 mg/L, p<0.01).

OW and NW group children had similar fasting blood glucose (87.5±4.9 vs 87.0±8.3 mg/dL) and HbA1C (5.4±0.3 vs 5.5±0.4 %) but higher fasting insulin (18.0±7.4 vs 11.7±5.3 uU/mL, p=0.02), higher area under the curve for insulin over glucose (1.1±0.6 vs. 0.6±0.3) and lower Whole-body Insulin Sensitivity Index (WBISI) (2.8±1.2 vs 4.8±2.2), p < 0.01 for all. Maternal pre-pregnancy BMI correlated with BMI percentile (r=0.38, p=0.02) and WBISI (r=-0.39, p=0.017) of offspring, adjusting for Tanner stage and BW percentile. Maternal pre-pregnancy BMI remained significantly related to the child’s WBISI after further adjusting for paternal BMI available in 22 children (r=-0.55, p=0.03).

Our results indicate that maternal pre-pregnancy BMI is a determinant of childhood BMI, its associated insulin resistance and adverse cardiometabolic profile. This effect appears to be independent of birth weight. Further studies are required to determine whether this pattern of transmission is the consequence of genetic or modifiable epigenetic factors, as opposed to familial aggregation of lifestyle risk factors.

Nothing to Disclose: HCT, JMR, JMC, FFB

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