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Obesity and Clinical Diabetes Research Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Phoenix, Arizona 85016
Address all correspondence and requests for reprints to: Joy C. Bunt, M.D., Ph.D., Obesity and Clinical Diabetes Research Section, National Institutes of Health, 4212 North 16th Street, Room 541-A, Phoenix, Arizona 85016. E-mail: jbunt{at}mail.nih.gov.
Context/Objective: Given the increasing rates of both childhood obesity and type 2 diabetes (T2DM), we investigated whether maternal diabetes status during pregnancy is a determinant of risk factors associated with T2DM or cardiovascular disease in offspring during childhood.
Design/Participants: Forty-two Pima Indians, aged 711 yr, were identified retrospectively from maternal oral glucose tolerance tests as offspring of a diabetic pregnancy (22 ODM, eight males, 14 females) or offspring born before the mother developed diabetes (20 PRE, 12 males, eight females).
Setting/Main Outcome Measures: Weight, height, body mass index, percent body fat, blood pressure, and fasting concentrations of glucose, insulin, hemoglobin A1c (HbA1c), total cholesterol, triglycerides, and high-density lipoprotein-cholesterol were measured while staying in an in-patient clinical research unit and compared in cross-sectional analyses.
Results: After adjustment for age and gender, ODM had significantly higher concentrations of HbA1c (ODM = 5.7 ± 0.4, PRE = 5.0 ± 0.4%, P = 0.002), higher systolic (SBP) blood pressure (ODM = 118 ± 13, PRE = 107 ± 10 mm Hg; P = 0.02), and lower concentrations of high-density lipoprotein (ODM = 41 ± 9, PRE = 48 ± 6 mg/dl, P = 0.03) than PRE. Maternal diabetes status during pregnancy persisted as a significant determinant of SBP (beta = 7.50, P = 0.03) and HbA1c (beta = 0.43, P = 0.002), independent of age, gender, and percent body fat.
Conclusion: Intrauterine exposure to diabetes is a significant determinant of higher SBP and HbA1c during childhood, independent of adiposity and a genetic predisposition to T2DM. These data suggest that in utero exposure to diabetes confers an additional independent risk for the development of T2DM and/or cardiovascular disease later in life.
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