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Background/Aim: Visceral adipose tissue plays a pivotal role in the pathogenesis of metabolic syndrome. Several investigations refer to the physiology of subcutaneous and visceral adipose tissue of adult obese subjects, focusing on the characterization of adipose-derived stem cells and their differentiation capacity. To date, no study has been carried out on visceral adipose tissue of children, the main limitation being the amount of fat tissue available. The aim of this investigation was to establish a method to successfully isolate adipose progenitor cells from very small specimens of omental fat obtained from children undergoing abdominal surgery. Methods: A previously described procedure employed to extract adipose progenitors from large amounts of lipoaspirate was modified. 0.5-cm3 specimens of omental fat were collected from 13 children and 2 newborns. Primary, secondary and higher passaged adipocytic progenitor cell cultures were established. Immunophenotyping of the generated lines was carried out by flow cytometry analysis. Differentiation experiments concerning the adipogenic phenotype were conducted. Results: A feasible method for isolating adipose progenitors from pediatric specimens of omental fat was established. Cells showed a fibroblast-like appearance consistent with that of mesenchymal stem cells obtained from bone marrow. The mesenchymal phenotype was confirmed by the surface antigenic profile of these cells. Cells also underwent adipogenic differentiation in vitro. Conclusion: The availability of progenitor primary cell lines from omental adipose tissue of children may allow future investigations aimed at unraveling whether fetal programming of adipogenesis is responsible for the pathogenesis of the metabolic syndrome that develops during adulthood in subjects, born with low birth weight, typically showing central fat redistribution.

Aims: To investigate (a) the prevalence of insulin resistance in children with intrauterine growth retardation (IUGR); (b) whether catch-up growth is associated with a higher risk of insulin resistance; (c) the insulin-like growth factor (IGF) system status. Methods: 49 children with IUGR aged 9.1 ± 3.3 years underwent anthropometric measurements, and assessment of insulin resistance and IGF system parameters. A fasting glucose/insulin ratio (G/I) Results: 11/49 (22%) children had a G/I Conclusions: (a) Children with IUGR have a high prevalence of reduced insulin sensitivity; (b) postnatal catch-up growth is related to intrauterine growth and actual nutritional status; (c) insulin sensitivity status is not related to postnatal growth but to liver function; (d) IGF system is normal and not related to the insulin resistance parameters during childhood.