With the rising prevalence of
obesity and
type 2 diabetes (T2D) in obese children, it is becoming imperative to detect disturbed
glucose metabolism as early as possible in order to prevent T2D development.
SUBJECTS/METHODS: Cross-sectional study of 92 obese children (median age 11.7 years, 51% female) and 7 lean children (median age 11.4 years, 57% female) who underwent an oral
glucose tolerance test (OGTT) in a tertiary pediatric care center.
Glucose tolerance was assessed and different indices for β-cell function,
insulin sensitivity and insulin secretion were calculated.
RESULTS: Nineteen obese children were identified with
prediabetes (PD, 12
impaired glucose tolerance, 4 increased fasting
glucose and 3 combined). Compared with the 73 obese children with normal
glucose tolerance (nGT), subjects with PD had higher
insulin resistance, but lower
insulin sensitivity and β-cell function, although their
glycated hemoglobin (HbA1c) levels were comparable. The Whole Body
Insulin Sensitivity Index (WBISI) and β-cell function by Insulin Secretion-Sensitivity Index-2 (ISSI-2) strongly correlated with the OGTT
glucose area under the curve 0-120 min (r = 0.392, p < 0.0002; r = 0.547, p < 0.0001, respectively). When testing the relation between early
insulin response during OGTT by insulinogenic index and
insulin sensitivity assessed by WBISI, a hyperbolic relationship between insulin secretion and
insulin sensitivity was found. The calculated disposition index was lower in subjects with PD vs. nGT (median 459 vs. 792, p = 0.004). We identified the OGTT 30-min/120-min
insulin ratio as a simple marker, which is significantly lower in obese children with vs. without PD (median 0.87 vs. 1.29, p = 0.021) and which has a better sensitivity and specificity for detecting PD than HbA1c among obese children.
CONCLUSIONS: Children with identified PD had changes of several markers for β-cell function,
insulin sensitivity and resistance before changes in HbA1c occurred. The lower disposition index indicates that these children have already inadequate β-cell compensation for the degree of
insulin resistance.