Three-Year Glycemic Trajectories in Subgroups With Type 1 Diabetes at Risk for Suboptimal Glycemic Control: A Multicenter Continuous Glucose Monitoring Study

OBJECTIVE To examine 3-year longitudinal trajectories of continuous glucose monitoring (CGM) metrics across subgroups at risk for suboptimal glycemic control among adults with type 1 diabetes. RESEARCH DESIGN AND METHODS In this multicenter study, 1,028 individuals contributed 3,441 longitudinal CGM profiles. Participants were stratified on the basis of age, chronic kidney disease (CKD), β-cell function, BMI, and triglyceride-glucose (TyG) tertile. Linear mixed-effects models were used to estimate subgroup differences in longitudinal changes. RESULTS At baseline, there was more time spent with glucose above target range, >180 mg/dL, for the subgroups of older age, CKD, severe β-cell failure, higher BMI, and highest TyG tertile (all P < 0.05), while severe β-cell failure was additionally associated with more time spent with glucose below target range (TBR), <70 mg/dL, along with greater glycemic variability (all P < 0.001). In relation to younger individuals, for older adults improvement in time spent with glucose in target range (TIR), 70–180 mg/dL, was comparable (β = 0.110; P = 0.102) and lower TBR was maintained (3.5% vs. 1.7%, respectively; P < 0.001). Among the CKD group significant improvement in TIR was seen (β = 0.228; P = 0.002) without exacerbation of hypoglycemia. Severe β-cell failure attenuated TIR improvement (β = −0.119; P = 0.025) and TBR reduction (β = 0.046; P < 0.001). Lower absolute TIR was seen for those with higher BMI and those in the highest TyG tertile. Greater TIR improvement was observed for those in the highest TyG tertile (β = 0.083; P = 0.001). CGM metrics varied widely within these subgroups. CONCLUSIONS Older age and CKD were associated with longitudinal glycemic improvement without worsening of hypoglycemia, whereas severe β-cell failure limited glycemic gains; substantial within-group heterogeneity supports individualized glycemic targets informed by CGM trajectories in type 1 diabetes.