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].
CITATION STYLE
Franchini, S., Blasetti, A., & Chiarelli, F. (2016). Nutrition and insulin resistance during 9 childhood and adolescence. In Research into Childhood-Onset Diabetes: From Study Design to Improved Management (pp. 101–113). Springer International Publishing. https://doi.org/10.1007/978-3-319-40242-0_9
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