Oral insulin administration and residual beta-cell function in recent-onset type 1 diabetes: a multicentre randomised controlled trial

Citation
L. Chaillous et al., Oral insulin administration and residual beta-cell function in recent-onset type 1 diabetes: a multicentre randomised controlled trial, LANCET, 356(9229), 2000, pp. 545-549
Citations number
30
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
LANCET
ISSN journal
01406736 → ACNP
Volume
356
Issue
9229
Year of publication
2000
Pages
545 - 549
Database
ISI
SICI code
0140-6736(20000812)356:9229<545:OIAARB>2.0.ZU;2-3
Abstract
Background Oral administration of autoantigens can slow the progression of beta-cell destruction in non-obese diabetic mice. We investigated whether o ral administration of recombinant human insulin could protect residual beta -cell function in recent-onset type 1 diabetes. Methods We enrolled 131 autoantibody-positive diabetic patients aged 7-40 y ears within 2 weeks of diagnosis (no ketoacidosis at diagnosis, weight loss <10%, polyuria for <6 weeks). They were randomly assigned 2.5 mg or 7.5 mg oral insulin daily or placebo for 1 year, in addition to subcutaneous insu lin therapy, Serum C-peptide concentrations were measured in the fasting st ate and after stimulation, to assess beta-cell function. Autoantibodies to beta-cell antigens were assayed. Analyses were by intention to treat. Findings Baseline C-peptide and haemoglobin A(1c) concentrations were simil ar in the three groups. During follow up, there were no differences between the groups assigned 2.5 mg or 7.5 mg oral insulin or placebo in subcutaneo us insulin requirements, haemoglobin A(1c) concentrations, or measurements of fasting (mean at 12 months 0.18 [SD 0.17], 0.17 [0.17], and 0.17 [0.12] nmol/L) or stimulated C-peptide concentrations (glucagon-stimulated 0.39 [0 .38], 0.37 [0.39], and 0.33 [0.24] nmol/L; meal-stimulated 0.72 [0.60], 0.4 9 [0.49], and 0.57 [0.51 nmol/L]. Neither age nor C-peptide concentration a t entry influenced treatment effects. No differences were seen in the time- course or titres of antibodies to insulin, glutamic acid decarboxylase, or islet antigen 2, Interpretation At the doses used in this trial, oral administration of insu lin initiated at clinical onset of type 1 diabetes did not prevent the dete rioration of beta-cell function.