Thus, our data imply that components of the GH axis might be involved in AT development and function in children and that a local obesity-related decrease of GHR, IGF-1 and IGFBP-3 expression in AT might contribute to AT dysfunction such as impaired adipogenic differentiation and adipocyte hypertrophy and may lead to a deterioration of the metabolic state. This evidence concerns the gene IGF1 and obesity due to melanocortin 4 receptor deficiency.