High Residual beta-cell Function in Chinese Patients With Autoimmune Type 1 Diabetes

Objective The destruction of pancreatic beta cells causes type 1 diabetes mellitus (T1D), an autoimmune disease. Studies have demonstrated that there is heterogeneity in residual beta-cell function in Caucasians; therefore, we aimed to evaluate beta-cell function in Chinese autoimmune T1D patients. Methods beta-cell function was determined using oral glucose tolerance testing or standardized steamed bread meal tolerance test in 446 participants with autoantibody-positive T1D. Clinical factors, such as age onset, sex, duration, body mass index, autoantibodies, other autoimmune diseases, diabetic ketoacidosis, hypoglycemia events, glycosylated hemoglobin, and insulin dose, were retrieved. We also analyzed single nucleotide polymorphism (SNP) data for C-peptides from 144 participants enrolled in the Chinese-T1D genome-wide association study. Results Of 446 T1D patients, 98.5%, 97.4%, 86.9%, and 42.6% of individuals had detectable C-peptide values (>= 0.003 nmol/L) at durations of < 1 year, 1 to 2 years, 3 to 6 years, and >= 7 years, respectively. A total of 60.7% of patients diagnosed at >= 18 years old and 15.8% of those diagnosed at < 18 years had detectable C-peptide after >= 7 years from the diagnosis. Furthermore, the patients diagnosed at >= 18 years old had higher absolute values of stimulated C-peptide (>= 0.2 nmol/L). Diabetic ketoacidosis, hypoglycemia events, and insulin doses were shown to be associated with beta-cell function. SNPs rs1770 and rs55904 were associated with C-peptide levels. Conclusion Our results have indicated that there are high residuals of beta-cell mass in Chinese patients with autoimmune T1D. These findings may aid in the consideration of therapeutic strategies seeking prevention and reversal of beta-cell function among Chinese T1D patients.