Residual β-cell function and glycemic control in young users of advanced hybrid closed loop systems: a retrospective study

Introduction: Persistent C-peptide secretion, indicating residual β-cell function, is present in ~29% of individuals with type 1 diabetes (T1D) and is inversely associated with age at onset and disease duration. It has been linked to reduced insulin needs and lower HbA1c but also to an increased risk of severe hypoglycemia. Objectives: This study examines C-peptide in users of advanced hybrid closed-loop (a-HCL) systems. Methods: A retrospective study was conducted on 52 children and adolescents with T1D (27 females) using the Medtronic Minimed 780G a-HCL system, who underwent non-fasting C-peptide evaluation. Data included age, sex, age at diagnosis, disease duration, HbA1c, and C-peptide from clinical reports, while daily insulin requirement, GMI, TIR, TAR, and TBR were extracted from device data covering the last two weeks. Statistical analyses included the Wilcoxon rank-sum test, chi-square test, and logistic regression. Results: Detectable C-peptide was found in 13 individuals (25%). These individuals had a higher age at diagnosis and shorter disease duration than those with undetectable C-peptide. HbA1c was slightly higher in those with detectable C-peptide, though not statistically significant. However, individuals with undetectable C-peptide had a significantly higher TBR (p=0.025). Logistic regression identified higher age at onset (β = 0.559, p = 0.008) and shorter disease duration (β = -1.099, p = 0.020) as significant predictors of detectable C-peptide, while HbA1c approached significance (β = 2.027, p = 0.056). Conclusions: Detectable C-peptide was present in 25% of children and adolescents with T1D using a-HCL and was associated with later onset and shorter disease duration, reinforcing prior findings. Among a-HCL users, HbA1c was similar regardless of C-peptide status, though detectable C-peptide was paradoxically linked to increased time below range. Further research is needed to clarify the clinical impact of residual β-cell function in a-HCL therapy.