Insulin resistance and obesity in childhood

Abstract

Childhood obesity is a significant health problem that has reached epidemic proportions around the world and is associated with several metabolic and cardiovascular complications. Insulin resistance is a common feature of childhood obesity and is considered to be an important link between adiposity and the associated risk of type 2 diabetes and cardiovascular disease. Insulin resistance is also a key component of the metabolic syndrome, and its prevalence in the paediatric population is increasing, particularly among obese children and adolescents. Several factors are implicated in the pathogenesis of obesity-related insulin resistance, such as increased free fatty acids and many hormones and cytokines released by adipose tissue. Valid and reliable methods are essential to assess the presence and the extent of insulin resistance, the associated risk factors and the effect of pharmacological and lifestyle interventions. The two most common tests to assess insulin resistance are the hyperinsulinemic euglycemic clamp and the frequently sampled i.v. glucose tolerance test utilizing the minimal model. However, both these tests are not easily accomplished, are time consuming, expensive and invasive. Simpler methods to assess insulin resistance based on surrogate markers derived from an oral glucose tolerance test or from fasting insulin and glucose levels have been validated in children and adolescents and widely used. Given the strong association between obesity, insulin resistance and the development of metabolic syndrome and cardiovascular disease, prevention and treatment of childhood obesity appear to be essential to prevent the development of insulin resistance and the associated complications.European Journal of Endocrinology 159 S67-S74

Critical periods and growth patterns from fetal life onwards associated with childhood insulin levels

“…It has been proposed that adverse exposures during fetal life lead to reduced muscle mass, reduced muscle sensitivity to insulin, and changes in the structure and function of the beta cells, which may subsequently lead to insulin resistance and beta cell dysfunction in later life [28][29][30]. Since only childhood growth characteristics were related to childhood insulin and Cpeptide levels in our study, the mechanisms underlying these associations may involve differences in the body composition of the child, for example an increased body fat mass resulting from rapid postnatal growth or genetic influences, rather than developmental adaptations during fetal life [21,[31][32][33]. However, it is possible that associations of fetal growth with insulin or glucose metabolism become apparent later in life.…”

Daily sugar-sweetened beverage consumption and insulin resistance in European adolescents: the HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) Study

“…3?5 (3) . IR in children and adolescents has been associated with CVD and metabolic disorders such as hypertension, dyslipidaemia, hepatic steatosis and endothelial dysfunction (6,7) . All of these risk factors can track into adulthood, increasing the risk of cardiovascular morbidity and mortality (8,9) .…”

Relationship of Waist Circumference with Lipid and Glucose Metabolism among Southern Brazilian Children

“…Visceral fat has a larger lipolitic function compared to subcutaneous fat, issuing a larger amount of free fat acids and glycerol, which are directed to the liver, starting a series of changes in lipid metabolism. In addition, adipose tissue has a prominent role in IR pathogenesis due to the liberation of metabolites and hormones that affect different stages of insulin action (Chiarelli & Marcovecchio, 2008 Despite the difficulty to establish the diagnosis of these RFs, it is critical to stress the importance of identifying children and adolescents that meet the requirements for this diagnosis, as they have higher metabolic risk and must be properly followed up. Continuity of these changes may favor the development of diabetes mellitus type 2 and occurence of CVD in adult life (Cavali, Escrivão, Brasileiro, & Taddei, 2010).…”