These Yale researchers reported the prevalence of impaired glucose tolerance in a cohort of 167 obese children and adolescents referred to an obesity clinic between 1999 and 2001. Patients were assessed as obese if their body mass index (BMI) was higher than the 95th percentile for age and sex. Impaired glucose tolerance was defined according to American Diabetes Association guidelines. Impaired glucose tolerance was detected in 25% of the 55 obese children (aged 4 to 10) and 21% of the 112 obese adolescents (aged 11 to 18). Silent type II diabetes was additionally identified in 4 percent of the obese adolescents. Impaired oral glucose tolerance was associated with insulin resistance while beta-cell function was still relatively preserved. Overt type II diabetes was linked to beta-cell failure.
Comparing patients with normal and impaired glucose tolerance, fasting and 30-minute plasma glucose levels were similar in the 2 groups of children but statistically significantly higher in adolescents with impaired glucose tolerance. While fasting hyperglycemia detected all 4 adolescents with diabetes, it was a very insensitive test in this study for detecting impaired glucose tolerance in children and adolescents. Fasting proinsulin levels were nearly twice as high in patients with impaired glucose tolerance (P<.001). Insulin resistance was noted to be the most important risk factor linked to the development of impaired glucose tolerance in severe childhood obesity (P<.001). Higher BMI was associated with impaired glucose tolerance and diabetes in the adolescents (P<.001 for both). The authors noted that 40% of the obese adolescent girls in this study had hirsutism, oligomenorrhea, and increased levels of total testosterone, findings consistent with the presence of polycystic ovary syndrome (PCO), and 35% of these girls had impaired glucose tolerance or overt diabetes.
Limitations of the study were the small sample size of subjects who were followed to confirm the diagnosis of impaired glucose tolerance and the fact that only a few patients were followed for several years to document transformation of impaired glucose tolerance to diabetes.
The study was well designed and executed, and standard statistical analysis supports its key findings. The patients enrolled were extreme examples of obesity and thus, the study did not address the greater overweight pediatric/adolescent population. The accompanying editorial1 addresses the points we should be aware of: 1) obesity during childhood is on the rise world-wide; 2) the risks of long-term obesity have been well established and include hypertension, hyperlipidemia, diabetes, respiratory disease, and cardiovascular morbidity; and 3) this study links obesity with impaired glucose tolerance. For adolescent girls, the association between obesity and PCO should not be lost. It has long been thought that weight gain may be a co-factor in the development of PCO, and PCO associated with obesity has been linked to reduced fertility.2