Serum adiposity-induced biomarkers in obese and lean children with recently diagnosed autoimmune type 1 diabetes

The incidence of childhood obesity is rising worldwide (1, 2). The prevalence of obesity and overweight is 32% in children from the general population (1), 35% in children with established type 1 diabetes (3), and 25% at the onset of pediatric type 1 diabetes, despite the weight loss that often precedes diagnosis (4, 5). Obesity increases the risk of cardiovascular disease and microvascular diabetic complications in adults and adolescents with type 1 diabetes (6–9). Obesity represents a state of chronic inflammation (10, 11), and obesity-induced inflammation has been associated with the development of components of the metabolic syndrome and of type 2 diabetes (12). A potential link between obesity and inflammation are adipokines, substances secreted by adipose tissue, such as adiponectin (13), leptin (14), omentin (15), resistin (16, 17), chemerin (18), and visfatin (19). Both proinflammatory adipokines, e.g., leptin and resistin, and anti-inflammatory adipokines, e.g., adiponectin and omentin, play critical roles in the regulation of inflammation (11). Children with type 1 diabetes are known to have an abnormal adipokine profile (20–23). However, the relationship between obesity and markers of adiposity and inflammation at the onset of autoimmune type 1 diabetes in children, especially under the age of 10 yr, has not been well characterized. Our aim was to compare circulating levels of a novel panel of adipokines and inflammatory cytokines associated with obesity in obese and lean children at the onset of autoimmune type 1 diabetes.