In 1998, the World Health Organization (WHO) designated obesity as a global epidemic affecting adults and children. In general, obesity is defined as the degree of somatic overweight that affords detrimental health consequences. This definition does not contemplate a specific cutoff point, but it allows health care providers to consider individual predisposition when assessing at-risk children, including underlying conditions, family history, medications, and lifestyle. Within the scientific community, the discovery of leptin and the elucidation of disorders affecting various neuroendocrine pathways and the genetic linkages of obesity have promulgated the notion that obesity is a disease. BMI is the accepted measure of obesity in children and adolescents. In childhood, comparison of BMI to normal curves for age and sex allows for categorization of BMI above the 85th percentile as overweight and above the 95th percentile as obese. In the United States, the most recent estimates of obesity prevalence are based on data from the 1999-2000 National Health and Nutrition Examination Survey (NHANES IV). 1 NHANES IV demonstrated that 20.6% of 2-to 5-year-old children in the United States were overweight. In older children, this prevalence was even higher, with 30.3% of 6-to 11-year-old children and 30.4% of adolescents (12-19 years of age) being overweight. The prevalence of obesity among children aged 0-23 months, 2-5 years, 6-11 years, and adolescents was 11.4, 10.4, 15.3, and 15.5%, respectively. This epidemic equally affects both sexes, and its prevalence has increased compared to data from the previous NHANES reports in all age ranges and racial groups. However, minorities are over-represented in this epidemic. 1 For instance, the prevalence of obesity among African-American (23.6%) and Hispanic (23.4%) adolescents is twice that among white adolescents (12.7%), and the rate of increase in the prevalence of obesity among African-American and Hispanic adolescents almost doubled between the periods 1988-1994 and 1999-2000, from 13.4 to 23.6% in African Americans and from 13.8 to 23.4% in Hispanics. Obesity has overtaken AIDS and malnutrition as the top health problem in the world. 2 Obesity markedly reduces life expectancy, especially among younger individuals. Severely obese (BMI > 45 kg/m 2) young adults have a reduced life expectancy of 5-20 years. Childhood obesity often persists into adulthood and has been independently associated with subsequent morbidity and mortality in adulthood. However, the sequelae of obesity are not limited to adulthood,

OBJECTIVE -Compared with Caucasians, obese African-American adolescents have a higher risk for type 2 diabetes. Subclinical inflammation and reduced glucagon-like peptide 1 (GLP-1) concentration are linked to the pathogenesis of the disease. We determined the relationship between insulin resistance, ␤-cell activity, and subclinical inflammation with GLP-1 concentrations and whether racial disparities in GLP-1 response were present in 49 obese adolescents (14 Ϯ 3 years; 76% African American; 71% female). RESEARCH DESIGN AND METHODS -Subjects underwent physical examinationand an oral glucose tolerance test. We measured levels of high-sensitivity CRP (CRP hs ), fibrinogen, glucose, GLP-1 total , GLP-1 active , and insulin. Insulin and glucose area under the curve (AUC), insulinogenic index (⌬I30/⌬G30), and composite insulin sensitivity index (CISI) were computed. Subjects were categorized by race and as inflammation positive (INFϩ) if CRP hs or fibrinogen were elevated.RESULTS -No racial differences were seen in mean or relative BMI. Thirty-five percent of subjects had altered fasting or 2-h glucose levels (African American vs. Caucasian, NS), and 75% were INFϩ (African American vs. Caucasian, P ϭ 0.046). Glucose and insulin, CISI, and ⌬I30/⌬G30 values were similar; African Americans had lower GLP-1 total AUC (P ϭ 0.01), GLP-1 active at 15 min (P ϭ 0.03), and GLP-1 active AUC (P ϭ 0.06) and higher fibrinogen (P ϭ 0.01) and CRP hs (NS) compared with Caucasians.

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