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Keywords:

  • latent autoimmune diabetes in adults;
  • thiazolidinediones;
  • insulin;
  • islet β cell function;
  • therapy

Abstract

Background

LADA is thought to result from the chronic autoimmune destruction of the insulin-producing pancreatic β cells. In addition to antidiabetic effects, the newly developed insulin sensitizer-thiazolidinediones have the potential to increase the insulin content of islet cells by downregulating local inflammation and autoimmune response. Therefore, we hypothesized that LADA patients might benefit from thiazolidinediones treatment.

Methods

LADA patients, with a fasting C-peptide (FCP) of 0.3 nmol/L or more, were enrolled and randomly assigned to receive subcutaneous insulin alone (insulin group, n = 12) or rosiglitazone plus insulin (insulin + RSG group, n = 11) to compare the impacts on islet β cell function. Plasma glucose, HbA 1c, fasting C-peptide (FCP) and C-peptide after 2 h 75-g glucose load (PCP) were determined every 6 months. GAD-Ab and C-peptide were measured with radioimmune assays. Islet β cell function was evaluated by PCP and ΔCP(ΔCP = PCP-FCP).

Results

All of the 23 patients have been followed up for 6 months, 17 cases for 12 months and 14 for 18 months. (1) During 6 months' follow-up, there were no significant changes for ΔCP and PCP levels in both groups. (2) PCP and ΔCP levels in insulin + RSG group patients stayed steady during the 12 months' observation (P = 0.161 for both PCP and ΔCP), while in the insulin alone group, both FCP (P = 0.021) and PCP (P = 0.028) levels decreased significantly. Furthermore, PCP (P = 0.004) and ΔCP(P = 0.015) differences between 12th month and baseline were higher in insulin + RSG group than those in the insulin group. (3) When observed up to 18 months, PCP and ΔCP levels in insulin + RSG group patients still stayed steady, while PCP and ΔCP levels decreased more in the insulin alone group.

Conclusions

This pilot study suggests that rosiglitazone combined with insulin may preserve islet β cell function in LADA patients. Copyright © 2004 John Wiley & Sons, Ltd.