American Diabetes Association
Browse
1/1
2 files

Clinical Impact of Residual C-Peptide Secretion in Type 1 Diabetes on Glycemia and Microvascular Complications

figure
posted on 2020-12-10, 20:30 authored by Anita Jeyam, Helen Colhoun, Stuart McGurnaghan, Luke Blackbourn, Timothy J McDonald, Colin N A Palmer, John A McKnight, Mark W J Strachan, Alan W Patrick, John Chalmers, Robert S Lindsay, John R Petrie, Sandeep Thekkepat, Andrew Collier, Sandra MacRury, Paul M McKeigue, SDRNT1BIO investigators
Objective: To quantify the relationship of residual C-peptide secretion to glycemic outcomes and microvascular complications in type 1 diabetes.

Design and Methods: C-peptide was measured in an untimed blood sample in the SDRNT1BIO cohort of 6076 people with type 1 diabetes followed for an average of 5.2 years.

Results: In regression models adjusted for age at onset and duration, effect sizes for C-peptide ≥200 versus <5 pmol/l were as follows: insulin dose at baseline 27% lower (p=2×10−39), HbA1c during follow-up 4.9 mmol/mol lower (p=3×10−13), hazard ratio for hospital admission for diabetic ketoacidosis during follow-up 0.44 (p=0.0001), odds ratio for incident retinopathy 0.51 (p=0.0003). Effects on risk of serious hypoglycemic episodes were detectable at lower levels of C-peptide, and the form of the relationship was continuous down to the limit of detection (3 pmol/l). In regression models contrasting C-peptide 30 to <200 with <5 pmol/l, the odds ratio for self-report of at least one serious hypoglycemic episode in the last year was 0.56 (p=6×10−8), and the hazard ratio for hospital admission for hypoglycemia during follow-up was 0.52 (p=0.03).

Conclusion: These results in a large representative cohort suggest that even minimal residual C-peptide secretion could have clinical benefit in type 1 diabetes, in contrast to a follow-up study of the DCCT intensively-treated cohort where an effect on hypoglycemia was seen only at C-peptide levels ≥130 pmol/l. This has obvious implications for design and evaluation of trials of interventions to preserve or restore pancreatic islet function in type 1 diabetes.

Funding

The establishment of the SDRN Type 1 Bioresource was supported by the Chief Scientist Office of the Scottish Government Health and Social Care Directorates [ETM/47] by Diabetes UK [10/0004010], and by in-kind contributions from the Scottish Diabetes Research Network to facilitate recruitment. The funding bodies had no role in the design, conduct or reporting of this study.

History

Usage metrics

    Diabetes Care

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC