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Obese Children with Low Birth Weight Demonstrate Impaired β-Cell Function during Oral Glucose Tolerance Test

Bambino Gesù Children’s Hospital-Istituto di Ricovero e Cura a Carattere Scientifico (C.B., A.G., D.F., P.I.P., G.U., M.C.), Department of Paediatric Medicine, Endocrinology, and Diabetes Unit, Epidemiology Unit (A.T.), and Laboratory of Molecular Endocrinology and Diabetes (V.N., F.B.), 00165 Rome, Italy; University of Tor Vergata (O.P., F.B.), Department of Internal Medicine, 00134 Rome, Italy; and San Raffaele Biomedical Park Foundation (F.B.), 00134 Rome, Italy

Address all correspondence and requests for reprints to: Claudia Brufani, M.D., Bambino Gesù Children’s Hospital–Istituto di Ricovero e Cura a Carattere Scientifico, Department of Pediatric Medicine, Endocrinology, and Diabetes Unit, Piazza S. Onofrio 4, 00165 Rome, Italy. E-mail: cbrufani{at}libero.it.

Objective: Epidemiological studies have shown an association between birth weight and future risk of type 2 diabetes, with individuals born either small or large for gestational age at increased risk. We sought to investigate the influence of birth weight on the relation between insulin sensitivity and β-cell function in obese children.

Subjects and Methods: A total of 257 obese/overweight children (mean body mass index-SD score, 2.2 ± 0.3), aged 11.6 ± 2.3 yr were divided into three groups according to birth weight percentile: 44 were small for gestational age (SGA), 161 were appropriate for gestational age (AGA), and 52 were large for gestational age (LGA). Participants underwent a 3-h oral glucose tolerance test with glucose, insulin, and C-peptide measurements. Homeostasis model of assessment for insulin resistance, insulinogenic index, and disposition index were calculated to evaluate insulin sensitivity and β-cell function. Glucose and insulin area under the curve (AUC) were also considered. One-way ANOVA was used to compare the three groups.

Results: SGA and LGA subjects had higher homeostasis model of assessment for insulin resistance than AGA subjects, but they diverged when oral glucose tolerance test response was considered. Indeed, SGA subjects showed higher glucose AUC and lower insulinogenic and disposition indexes. Insulin AUC was not different between groups, but when singular time points were considered, SGA subjects had lower insulin levels at 30 min and higher insulin levels at 180 min.

Conclusions: SGA obese children fail to adequately compensate for their reduced insulin sensitivity, manifesting deficit in early insulin response and reduced disposition index that results in higher glucose AUC. Thus, SGA obese children show adverse metabolic outcomes compared to AGAs and LGAs.