Interleukin-6 in Obese Children and Adolescents With and Without Glucose Intolerance

Abstract

In recent years, the increased prevalence of obesity in industrialized countries has been accompanied by a parallel rise in the incidence of type 2 diabetes, both in adults and children (1–3). Obese children and adults, after a period of time with obesity (4), may develop type 2 diabetes. Glucose intolerance, an intermediate stage in the progression toward type 2 diabetes, may become apparent in obesity (5,6). Insulin resistance in obese children frequently precedes the development of type 2 diabetes, metabolic syndrome, or both (7,8), and type 2 pre-diabetes has been reported in obese adolescents (9,10). The mechanisms implicated in insulin resistance in obese subjects remain to be fully established. Adipose tissue is the source of a wide variety of molecules involved in the regulation of energy output and carbohydrate metabolism. Among these, proinflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, in particular, appear to play a role in modulating insulin sensitivity in peripheral tissues and have been associated with the development of insulin resistance in adults (11). Furthermore, glucose induces oxidative stress and increased nuclear factor-κB binding, and it also increases the transcription of nuclear factor-κB–dependent proinflammatory genes (TNF-α and IL-6) (12,13). Early detection of subjects with obesity-associated metabolic disorders, especially those at risk for glucose intolerance, is …