Epidemiologic data provide evidence that the frequency of obesity and cardiometabolic risk factors shows an increasing tendency in childhood. Insulin resistance plays a central role in the pathogenesis of cardiovascular and metabolic consequences of obesity. Transient decrease in the insulin sensitivity during puberty is a well-known physiological process; however, the feature of this phenomenon is not clear in obese children with increased cardiometabolic risk.
Aim: The aim of the present study was to assess the effect of puberty on insulin resistance and metabolic parameters in obese children with and without increased cardiometabolic risk.
Materials and methods: Anthropometric data, insulin levels during oral glucose tolerance test and lipid status were analyzed of 161 obese children aged 4-18 years. Σinsulin/Σglucose ratio was obtained during glucose load and HOMA index was used to assess insulin resistance. Children were sorted into prepubertal (T1), pubertal (T2-4) and postpubertal (T5) cohorts according to Tanner staging criteria and metabolic and insulin resistance parameters were evaluated. Increased cardiometabolic risk was defined as the presence of any two risk factors (elevated fasting plasma glucose, blood pressure, triglyceride or decreased HDL-cholesterol) in addition to obesity.
Results: Out of 161 obese subjects, 43 (26.7%) had increased cardiometabolic risk. Decreased HDL-cholesterol and/or elevated triglyceride was observed in 101 (56.5%) cases. Impaired glucose tolerance and/or impaired fasting glucose was found in 23 (14.4%) cases. In subjects without increased cardiometabolic risk, the Σinsulin/Σglucose ratio in T1 stage was significantly lower than in T2-4 and T5 stages (p = 0.01). In children with increased cardiometabolic risk, the insulin/glucose ratio was similar in T1, T2-4 and T5 stages, however, it was significantly higher in T1 stage as compared to subjects without increased cardiometabolic risk (p = 0.04). In T2-4 and T5 stages, Σinsulin/Σglucose ratio did not differ between children with and without increased cardiometabolic risk. No difference was found in HOMA index between groups with and without increased cardiometabolic risk in T1 stage, however significantly higher levels were observed in subjects with increased cardiometabolic risk at T2-4 stages (p = 0.01), indicating the presence of fasting hyperinsulinemia in this cohort. Elevated HbA1c (≥6.0%) was found in 13 (16%) out of the 81 children investigated, of whom only two cases had abnormal oral glucose tolerance test. In cases having normal HbA1c, oral glucose tolerance test showed impaired glucose tolerance in 5 cases, impaired fasting glucose in 2 cases, both impaired glucose tolerance and impaired fasting glucose in 2 cases, and type 2 diabetes in 2 cases.
Conclusion: Increased insulin resistance can be observed in obese children without increased cardiometabolic risk. In obese children with increased cardiometabolic risk, substantial insulin resistance occurs in prepuberty and it is present at similar level throughout puberty. Fasting insulin levels are elevated in obese subjects with increased cardiometabolic risk as compared to those without increased cardiometabolic risk. To reveal type 2 diabetes cases, HbA1c and oral glucose tolerance test results should be assessed parallel.