Fall in C-Peptide During First 4 Years From Diagnosis of Type 1 Diabetes: Variable Relation to Age, HbA1c, and Insulin Dose

We aimed to describe the natural history of residual insulin secretion in Type 1 Diabetes TrialNet participants over 4 years from diagnosis and relate this to previously reported alternative clinical measures reflecting β-cell secretory function. Data from 407 subjects from 5 TrialNet intervention studies were analyzed. All subjects had baseline stimulated C-peptide values of ≥0.2 nmol/L from mixed-meal tolerance tests (MMTTs). During semiannual visits, C-peptide values from MMTTs, HbA1c, and insulin doses were obtained. The percentage of individuals with stimulated C-peptide of ≥0.2 nmol/L or detectable C-peptide of ≥0.017 nmol/L continued to diminish over 4 years; this was markedly influenced by age. At 4 years, only 5% maintained their baseline C-peptide secretion. The expected inverse relationships between C-peptide and HbA1c or insulin doses varied over time and with age. Combined clinical variables, such as insulin-dose adjusted HbA1c (IDAA1C) and the relationship of IDAA1C to C-peptide, also were influenced by age and time from diagnosis. Models using these clinical measures did not fully predict C-peptide responses. IDAA1C ≤9 underestimated the number of individuals with stimulated C-peptide ≥0.2 nmol/L, especially in children. Current trials of disease-modifying therapy for type 1 diabetes should continue to use C-peptide as a primary end point of β-cell secretory function. Longer duration of follow-up is likely to provide stronger evidence of the effect of disease-modifying therapy on preservation of β-cell function..

Medienart:	Artikel

Erscheinungsjahr:	2016
Erschienen:	2016

Enthalten in:	Zur Gesamtaufnahme - volume:39
Enthalten in:	Diabetes care - 39(2016), 10, Seite 1664-1670

Sprache:	Englisch

Beteiligte Personen:	Hao, Wei [VerfasserIn] Gitelman, Steven [Sonstige Person] DiMeglio, Linda A [Sonstige Person] Boulware, David [Sonstige Person] Greenbaum, Carla J [Sonstige Person]

Links:	Volltext www.ncbi.nlm.nih.gov

doi:	10.2337/dc16-0360

funding:
Förderinstitution / Projekttitel:

PPN (Katalog-ID):	OLC198470589X