Abstract
Insulin resistance could be defined as “the decreased tissue response to insulin-mediated cellular actions and is the inverse of insulin sensitivity [1].” A critical effect of insulin resistance is a delayed and unsuitable release of insulin after meals. Physiologic properties of insulin are impaired at normal plasma levels [2]. The incidence of insulin resistance during childhood and adolescence varies notably, according to gender and race [3]. Patients with insulin resistance store excess calories as fats and increase gluconeogenesis from proteins and fatty acids. This metabolic phenotype has been defined as “thrifty phenotype” and a multifactorial pathogenesis has been suggested [2]. However, there are conflicting data about the role of environmental and genetic factors, and several genetic loci remain controversial (see Table 9.1) [4–14].
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Franchini, S., Blasetti, A., Chiarelli, F. (2017). Nutrition and Insulin Resistance During Childhood and Adolescence. In: Scaramuzza, A., de Beaufort, C., Hanas, R. (eds) Research into Childhood-Onset Diabetes. Springer, Cham. https://doi.org/10.1007/978-3-319-40242-0_9
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