ESPE Abstracts

Background: Insulin resistance (IR) plays a larger role in type 1 diabetes (T1D) disease process than is commonly recognized. Dipeptidyl peptidase-4 (DPP-4) is an enzyme that is expressed on almost all cell surfaces. It deactivates many bioactive peptides involved in glucose regulation; glucose-dependent insulinotropic polypeptide and Glucagon-like peptide-1.

Objectives: This study evaluates serum DPP-4 activity in adolescent patients with T1D compared to controls and investigates the relationship between DPP-4 activity and the development of IR in these patients.

Subjects and Methods: We examined serum DPP-4 activity in 50 T1D adolescent patients following up in the outpatient clinic of Diabetes Endocrine Metabolism Pediatric Unit, Children Hospital, Cairo University and 80 healthy controls. All subjects were assessed for IR using the equation for estimated glucose disposal rate (eGDR). Biochemical evaluation including glycated haemoglobin (HbA1c) and lipid profile were performed.

Results: The mean age and diabetes duration of T1D patients were14.44 and 6.27 years, respectively. Our studied patients showed poor glycemic control with a mean value for HbA1c was 10.51%. IR was found in 80% of T1D patients (eGDR<9), and 34% of our patients were dyslipidemic.

A significant elevation of DPP-4 was found in the control group (P=0.04). T1D patients were classified into 3 groups according to serum DPP-4 tertiles (<2.3, 2.3-5.7, >5.7 ng/ml) there was a significant increase in BMI SDS (P=0.01) and total cholesterol (P=0.041) across the 3 groups. Significant correlation was only found between DPP-4 levels and insulin dose (P=0.024, r=0.318). DPP-4 level was found to be significantly higher in the group of patients with good glycemic control. No significant relation was found between DPP-4 activity and eGDR.

Conclusion: DPP-4 was found to be related to the state of adiposity rather than the diabetic process in adolescents with T1D. It seemed to beneficial rather than being harmful and require inhibition. Our patients were resistant to insulin but this resistance mostly related to poor glycemic control rather than their serum DPP-4 activity.