부산대학교 도서관

Objective: Glycemic control deteriorates more rapidly in youth vs adults. We compared model‐derived measures of β‐cell function between youth and adults with either impaired glucose tolerance (IGT) or type 2 diabetes to determine if a β‐cell defect differentiates these age groups. Methods: This is a cross‐sectional analysis of baseline data from the Restoring Insulin Secretion (RISE) Study. Youth (54 Y‐IGT, 33 Y‐D) and adults (250 A‐IGT, 104 A‐D) underwent 3‐hour oral glucose tolerance tests for modeling of insulin secretion rates (ISRs), glucose sensitivity, and rate sensitivity. Insulin sensitivity was quantified as the glucose infusion rate/insulin (M/I) from a hyperglycemic clamp. Results: Youth had lower insulin sensitivity despite similar body mass index. Analyses were adjusted for insulin sensitivity. Youth had higher basal ISRs (Y‐IGT 200 ± 161 vs A‐IGT 152 ± 74, P <.001; Y‐D 245 ± 2.5 vs A‐D 168 ± 115 pmol/min/m2, P =.007) and total ISRs (Y‐IGT 124 ± 86 vs A‐IGT 98 ± 39, P <.001; Y‐D 116 ± 110 vs A‐D 97 ± 62 nmol/m2, P =.002). Within IGT, glucose sensitivity (Y‐IGT 140 ± 153 vs A‐IGT 112 ± 70 pmol/min/m2/mM, P =.004) and rate sensitivity (median[interquartile range]:Y‐IGT 2271[1611, 3222] vs A‐IGT 1164[685, 1565] pmol/m2/mM, P <.001) were higher in youth, but not different by age group within diabetes. Conclusions: Model‐derived measures of β‐cell function provide additional insight into the pathophysiology of type 2 diabetes in youth with higher ISRs and β‐cell secretion more responsive to glucose in youth relative to adults even after adjusting for differences in insulin sensitivity. It is unknown whether these findings in youth reflect β‐cells that are healthier or whether this is a defect that contributes to more rapid loss of function. [ABSTRACT FROM AUTHOR]