Deborah A Elder1, Lindsey N Hornung2, Jane C Khoury3, David A D'Alessio4. 1. Department of Pediatrics, Division of Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. Electronic address: Deborah.elder@cchmc.org. 2. Department of Pediatrics, Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 3. Department of Pediatrics, Division of Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 4. Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; Department of Medicine, Cincinnati VAMC, Cincinnati, Ohio.
Abstract
PURPOSE: The progression of β-cell function in newly diagnosed adolescents with type 2 diabetes mellitus (T2DM) is not well documented. We hypothesized that at the time of diagnosis with T2DM, adolescents would have impaired β-cell function as demonstrated by the disposition index (calculated as: insulin secretion adjusted for insulin sensitivity), and this would be followed by a rapid decline of function despite standard medical management. METHODS: Thirty-nine adolescents with recently diagnosed T2DM and 32 obese adolescent controls with normal glucose tolerance had acute insulin response to glucose, homeostatic model assessment of insulin resistance, and disposition index measured serially over 2 years. RESULTS: In the adolescent T2DM group, fasting glucose increased over 2 years (p = .04), while DI was impaired at baseline and showed an overall relative decline of 25% per year. The mean Hemoglobin A1c remained below 8% (64 mmol/mol). Differences were observed between the T2DM and control adolescents in the way DI changed over time (p = .02). CONCLUSIONS: β-cell function in adolescents with recently diagnosed T2DM was impaired with no improvement of β-cell function over the 2 years of study despite stable Hemoglobin A1c, body mass index markers of insulin sensitivity, and standard treatment of hyperglycemia.
PURPOSE: The progression of β-cell function in newly diagnosed adolescents with type 2 diabetes mellitus (T2DM) is not well documented. We hypothesized that at the time of diagnosis with T2DM, adolescents would have impaired β-cell function as demonstrated by the disposition index (calculated as: insulin secretion adjusted for insulin sensitivity), and this would be followed by a rapid decline of function despite standard medical management. METHODS: Thirty-nine adolescents with recently diagnosed T2DM and 32 obese adolescent controls with normal glucose tolerance had acute insulin response to glucose, homeostatic model assessment of insulin resistance, and disposition index measured serially over 2 years. RESULTS: In the adolescent T2DM group, fasting glucose increased over 2 years (p = .04), while DI was impaired at baseline and showed an overall relative decline of 25% per year. The mean Hemoglobin A1c remained below 8% (64 mmol/mol). Differences were observed between the T2DM and control adolescents in the way DI changed over time (p = .02). CONCLUSIONS: β-cell function in adolescents with recently diagnosed T2DM was impaired with no improvement of β-cell function over the 2 years of study despite stable Hemoglobin A1c, body mass index markers of insulin sensitivity, and standard treatment of hyperglycemia.
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