AI Article Synopsis

  • The study investigates the link between persistent metabolic syndrome (MetS) and the risk of developing type 2 diabetes in overweight Hispanic children.
  • A total of 73 children, aged around 11 years, were categorized into three groups based on their MetS status over three years: Never (no MetS), Intermittent (some MetS), and Persistent (MetS consistently).
  • Findings show that the Persistent group experienced higher fat gain and an increased insulin response, along with lower insulin sensitivity and beta cell function, indicating a greater risk for type 2 diabetes.

Article Abstract

Objective: To examine an association between persistent metabolic syndrome (MetS) and the risk for type 2 diabetes in overweight Hispanic children.

Study Design: A total of 73 subjects (mean age, 11.0 +/- 1.7 years) from a longitudinal study were classified as Never (negative for MetS at all 3 annual visits), Intermittent (positive for MetS at 1 or 2 visits), or Persistent (positive for MetS at all 3 visits). Measures included dual-energy x-ray absorptiometry, magnetic resonance imaging, the 2-hour oral glucose tolerance test, and the frequently sampled intravenous glucose tolerance test.

Results: The Persistent group had a faster rate of fat mass gain than the Never group (20% vs 15% gain of baseline value; P < .05 for time *group interaction [time = visit]). Independent of body composition, the Persistent group increased by 70% in insulin incremental area under the curve, whereas the other groups decreased (P < .05 for time *group interaction). Despite no time *group interactions for insulin sensitivity, acute insulin response, or disposition index, the Persistent group maintained 43% lower insulin sensitivity (P < .01) and by visit 2 had a 25% lower disposition index (P < .05) compared with the Never group.

Conclusions: Patients with persistent MetS had accelerated fat gain, increased insulin response to oral glucose, and decreased sensitivity and beta cell function, indicators of progressively greater risk for type 2 diabetes.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709847PMC
http://dx.doi.org/10.1016/j.jpeds.2009.04.008DOI Listing

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