No evidence for a major β-cell dysfunction in young adults born with intra-uterine growth retardation

Abstract

The association between low birth weight and the later development of type 2 diabetes is well established. It has been hypothesized that in utero undernutrition may affect pancreatic β‐cell development, leading to an impaired β‐cell function in adulthood. We have previously demonstrated that intrauterine growth retardation (IUGR) is associated with insulin‐resistance early in adulthood. The aim of this study was to test whether IUGR would affect β‐cell function in young adults. Twelve 25‐yr‐old insulin‐resistant subjects with IUGR were matched for age gender and body mass index (BMI) to 13 controls. All of them had normal glucose tolerance. Mean fasting plasma glucose did not significantly differ between the group with IUGR and the control group (97 ± 7 vs. 98 ± 4 mg/dL; p = 0.83). Blood glucose was maintained at 124.8 ± 6.5 vs. 126.2 ± 7.5 mg/dL above the basal glycemia in the IUGR and control groups (p = 0.64) throughout the hyperglycemic clamp. Serum insulin concentrations did not significantly differ between the group with IUGR and the control group either during the first (0–10 min) phase (311 ± 252 vs. 248 ± 184 pmol/L, p = 0.85) or during the second (80–100 min) phase (575 ± 284 vs. 559 ± 413 pmol/L, p = 0.72). C‐peptide concentrations were similar in both groups during the two phases (2.35 ± 1.44 vs. 2.59 ± 1.10 nmol/L, p = 0.39 and 4.86 ± 1.36 vs. 4.96 ± 1.41 nmol/L, p = 0.91). In conclusion, our data do not argue in favor of an impairment of β‐cell function at 25 yr of age as a consequence of in utero undernutrition, but rather suggest that insulin resistance might be the primary defect responsible for the development of metabolic disorders associated with IUGR in adulthood.