ESPE Abstracts

Background: The pathophysiology of type 2 diabetes mellitus (T2DM) is based on defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Young people have a more aggressive course of the disease. However, the impact and sequence of pathological mechanisms involved in the development of T2DM in adolescents hasn’t been established. Diagnosis of the prediabetes in time can be useful in prevention T2DM progression.

Aims: to study the role of pancreatic β-cell dysfunction and insulin resistance in the development of prediabetes in obese adolescents.

Materials: The Study included 95 obese adolescents. Inclusion criteria: SDS BMI≥2.0, Tanner stage ≥II, age <18.0 years, exclusion criteria: diabetes mellitus. The sample was divided into prediabetics (n=40, mean age 14,0±1,53 years; SDS BMI 3,1±0,54, boys n=23) and nonprediabetics (n=55, mean age 14,6±1,67 years; SDS BMI 3,1±0,54; boys n=32). Both groups were matched on age, SDS BMI, sex (P=0.082, P=0.975, P=0.947, respectively). Prediabetes in adolescents was diagnosed using American Diabetes Association criteria. The research included the estimate levels of insulin and c-peptide as well as the calculations of the HOMA-IR, HOMA-B and disposition index (DI). Data was analyzed by using SPSS Statistics for Windows, Version 26.0.

Results: There were statistically significant differences between indices of groups with prediabetes and nonprediabetics: HOMA-B (median 116.56; IQR [88.55-197.44] vs 217.85; [144.44-301.20] %, respectively; P<0.001), DI (median 35.68; IQR [30.35-47.57] vs 51.13; [44.04-88.56] %, respectively; P<0.001). The indices of fasting insulin (median 13.26; IQR [9.54-17.67] vs 15.19; [10.57-22.23] µIU/ml, respectively; P=0.263); c-peptide (median 1.87; IQR [1.46-2.27] vs 1.91; [1.41-2.49] ng/ml, respectively; P=0.582) and HOMA-IR (median 3.48; IQR [2.20-4.56] vs 3.16; [2.16-5.12], respectively; P=0.892) between the groups didn’t differ. Statistically significant logistic regression model was obtained for evaluating the dependence of the development of prediabetes on the HOMA-B, HOMA-IR, DI (P<0.001). The increase of HOMA-IR is a risk factor for developing prediabetes (odds ratio (OR) =1.7; 95% confidence interval (CI): 1.16-2.51). The decrease HOMA-B and DI by 1%, increased the chances of developing prediabetes in 1.01 times (odds ratio (OR) = 0.99; 95% (CI): 0.98-0.99) and 1.06 times (OR=0.94; 95% CI: 0.91-0.97), respectively.

Conclusions: Despite the fact that both groups had the equal level of insulin resistance, the impairment of β-cell function in prediabetics and nonprediabetics was too dissimilar. Hence, β-cell defect can be the main driving mechanism in youth-onset prediabetes and an unfavorable prognostic factor.