ESPE Abstracts

Background: The development of diabetes mellitus type 2 (T2DM) involves a disbalance between pancreatic β-cell function and insulin sensitivity. The impact and sequence of pathological mechanisms involved in the development of T2DM in adolescents haven’t been established.

Aims: To compare the role of pancreatic β-cell dysfunction and insulin resistance in the development of prediabetes and T2DM in obese adolescents.

Materials and Methods: We assigned 55 adolescents with obesity to have prediabetes or T2DM. Inclusion criteria: the presence of T2DM or prediabetes, SDS BMI ≥2.0, Tanner stage ≥II, age <18.0 years, exclusion criteria: other types of diabetes. The sample was divided into having prediabetes (n = 40) and T2DM (n = 15). Both groups were matched on SDS BMI (р=0,312); sex (P = 0,282) but they distinguished on age (р=0,016). Impaired carbohydrate metabolism was diagnosed using ADA criteria. The research included the estimate levels of glucose, insulin, c-peptide, ALT, AST, HbA1c, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides as well as the calculations of the HOMA-IR, HOMA-B, disposition index (DI) and TyG index.

Results: There were statistically significant differences between indices of groups with prediabetes and T2DM: fasting plasma glucose (5,63±0,49; 95% CI: 5,48-5,79 vs 8,29±2,07; 7,14-9,43 mmol/l; P <0,001); HbA1c (5,50±0,31; 5,39-5,59 vs 8,16±1,39; 7,39-8,93%; P <0,001), fasting insulin (13,26; IQR [9,54-17,67] vs 36,57; [15,56-44,61] µIU/ml; P = 0,001), c-peptide (1,87; [1,46-2,27] vs 3,58; [3,21-4,56] ng/ml; P <0,001). Comparing of the indirect methods for quantifying insulin resistance were statistically significant differences between ones: HOMA-IR (3,48; [2,20-4,56] vs 11,82; [4,90-16,73]; р<0,001); TyG index (8,63±0,46; 8,49-8,78 vs 9,39±0,68; 8,99-9,75; р<0,001) and 2hPG (7,04±0,93; 6,74-7,34 vs 14,01±3,19; 11,72-16,29 mmol/l; P <0,001). The level of indicators characterizing insulin sensitivity were significantly greater in the diabetes group than the prediabetes group such as triglycerides (1,63; [1,30-2,33] vs 1,25; [0,97-1,51] mmol/l; р=0,034) and ALT (75,00; [39,00-110,50] vs 20,6; [14,0-31,4]; U/l; P <0,001). Although the levels of total cholesterol (4,47±0,73; 4,23-4,72 vs 4,64±1,16; 3,99-5,28; mmol/l; P = 0,510); LDL-cholesterol (2,89±0,96; CI: 2,55-3,20 vs 2,84±0,71; 2,45-3,23; mmol/l; P = 0,891) and HDL-cholesterol (1,07±0,22; 1,00-1,15 vs 0,98±0,27; 0,83-1,13; mmol/l; P = 0,194) didn’t differ. The β-cell functional activity index (HOMA-B) between prediabetics (116,56; [88,55-197,44] and diabetics (122,12; [61,40-234,21] %; P = 0,865) was statistically comparable. However, DI in the prediabetes group were significantly higer (35,68; [30,35-47,57] than the T2DM group (13,91; [10,93-16,75] %; P <0,001).

Conclusion: The present comparative research showed that the leading mechanism of the transformation from prediabetes into T2DM is insulin resistance which can’t be compensated by insulin secretion.