OBJECTIVE: To examine the in¯uence of the macronutrient intake in early life on the development of overweight in children. DESIGN AND SUBJECTS: An ongoing longitudinal study including 147 randomized healthy children followed up from birth. MEASUREMENTS: Anthropometric parameters were measured at birth, 1 and 5 y of age. Dietary habits at the age of 1 and 5 were assessed by age-adjusted food-frequency questionnaires and 24 h recalls. Parents' body mass index (BMI) was also recorded. RESULTS: Parental overweight was observed for 51% children. The prevalence of overweight at the age of 5 y was higher in children with than without parental overweight (37.3% vs 8.3%, P`0.0001). Five-year old overweight children had a higher percentage intake of proteins at the age of 1 y than non overweight children (22% vs 20%, P 0.024) and lower intake of carbohydrates (44% vs 47%, P 0.031). Multiple logistic analysis con®rmed that protein intake at 1 y of age was associated with overweight at 5 y (P 0.05). In children born from overweight mothers, prevalence of overweight at the age of 5 y tended to be higher in bottle-fed than in breast-fed ones (62.5% vs 23.3%, P 0.08). CONCLUSION: Parental overweight is a major risk factor for childhood overweight in the ®rst years of life, but an early high protein intake may also in¯uence the development of adiposity.

Objective. While the role of osteoclasts in bone loss has been well investigated, the involvement of osteoblast-lineage cells has not been completely elucidated. Several genes contribute to normal osteoblastic differentiation from mesenchymal stem cells (MSCs), but an understanding of their role in the pathogenesis of osteoporosis is still lacking. The present study was undertaken to evaluate a possible alteration of osteogenic gene expression as a mechanism contributing to bone loss.Methods. We studied the osteogenic differentiation process in MSCs obtained from the peripheral blood of 31 patients with osteoporosis and 20 normal donors. The cells were evaluated by colony-forming unit-fibroblastic assay and cultured in osteogenic medium to analyze the transcription factors runt-related transcription factor 2 (RUNX-2) and Sp7 and the bone-related genes COL1A1, SPARC, and SPP1 after 3, 8, and 15 days of differentiation. In addition, to determine possible differences between the 2 groups in terms of osteoclastic and osteoblastic activation, we quantified the osteoprotegerin (OPG) and RANKL levels in the supernatants of osteoblastic culture.Results. Circulating MSCs were increased in osteoporosis patients compared with normal donors. In contrast, gene expression analysis revealed downregulation of RUNX2, Sp7, COL1A1, SPARC, and SPP1 in patients with osteoporosis, associated with a lower OPG:RANKL ratio.Conclusion. These results suggest that an alteration of osteoblastic differentiation may contribute to the pathogenesis of osteoporosis. The noninvasive approach used in the present study could be proposed as a useful tool for studying mesenchymal involvement in bone diseases.

Cbfa1/Runx2 is a bone transcription factor homologous to the Drosophila protein, Runt. Runx2 is a master gene that encodes for a protein involved in the osteogenic differentiation process from mesenchymal precursors. It is known that in Cbfa1 deficient mice (Cbfa1(-/-)) the lack of mature osteoblasts is associated to incomplete bone mineralization. An important aim of modern biology is the development of new molecular tools for identification of therapeutic approaches. Recent discoveries in cell and molecular biology enabled researchers in the bone tissue-engineering field to develop new strategies for gene and cell-based therapies. This review summarizes the process of osteogenic differentiation from mesenchymal stem cells and the importance of bone regeneration is discussed. In particular, given the increasing interest in the study of the transcription factor Runx2, this review highlights the role of this target gene and addresses recent strategies using Runx2 for bone regeneration.

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