![]() ![]() One Ab − patient had high levels of nonspecific binding in the insulin radioimmunoassay, and her insulin data were not included in this analysis. Insulin, C-peptide, glucagon, leptin, and adiponectin were measured using radioimmunoassay as before ( 9). ![]() Plasma glucose was measured with a glucose analyzer (Yellow Springs Instrument, Yellow Springs, OH). ![]() Subcutaneous abdominal adipose tissue (cm 2) All studies were approved by the University of Pittsburgh Institutional Review Board, and consents and assents were obtained prior to the investigation. None of the obese control subjects were on medications that affect blood glucose metabolism. The treatment modalities at the time of the study and the characteristics of the study population are summarized in Table 1. The control group consisted of 21 age-matched obese, otherwise healthy, adolescents recruited from the community. Islet cell antibodies were tested using the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)-sponsored harmonization assay. Islet cell antibody screening revealed 25 with negative antibodies and 11 with positive antibodies. Thirty-six obese adolescents, all reported previously ( 8), with CDx-type 2 diabetes diagnosis made by the attending endocrinologist based on the American Diabetes Association diagnostic criteria ( 1), were recruited from the Diabetes Center at the Children's Hospital of Pittsburgh. Therefore, in this study, we investigated whether the oral glucose tolerance test (OGTT), a clinically applicable tool, could be used to distinguish the differences in insulin sensitivity and secretion between the two groups of patients with phenotypic type 2 diabetes versus obese control subjects with normal glucose tolerance. While the clamp technique is considered the gold standard for studying in vivo insulin secretion and sensitivity, its use is limited to the research setting. These pathophysiological differences have important bearing on the management of diabetes and highlight the importance of making the correct diagnosis. Moreover, the Ab − CDx-type 2 diabetic patients had features consistent with the metabolic syndrome. While insulin sensitivity was severely impaired in Ab − but not Ab + patients, β-cell function was almost completely abolished in Ab + and not Ab − type 2 diabetes ( 8). ![]() In a previous study using the hyperinsulinemic-euglycemic and the hyperglycemic clamp, we demonstrated important distinguishing features in insulin sensitivity and secretion between antibody-positive (Ab +) versus -negative (Ab −) obese youth with a clinical diagnosis of type 2 diabetes (CDx-type 2 diabetes). Moreover, 10–75% of physician-diagnosed obese youth with type 2 diabetes have islet cell autoantibodies ( 3, 5, – 7), which is the hallmark of autoimmune type 1 diabetes. However, the increasing prevalence of obesity in children, including those newly diagnosed with type 1 diabetes, has made the clinical distinction between the two types of diabetes more difficult ( 4). The diagnosis of type 1 versus type 2 diabetes in children relies largely on the clinical presentation with obesity being a major characteristic of children diagnosed with type 2 diabetes ( 1, 2). While type 1 diabetes remains the most common form of childhood diabetes, type 2 diabetes in youth has increased worldwide over the last decade concomitant with the epidemic increase in childhood obesity ( 2, 3). Diabetes in youth is generally classified into two major categories: type 1 diabetes characterized by autoimmune destruction of the pancreatic β-cells and absolute insulin deficiency and type 2 diabetes characterized by insulin resistance coupled with a nonimmune-mediated β-cell failure and relative insulin deficiency ( 1). ![]()
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