Autoimmunity to the islets may lead to -cell dysfunction in type 2 diabetes (T2D). However, its frequency and clinical relevance have yet to be identified. For a study, researchers assessed the incidence of cellular and humoral islet autoimmunity in individuals with T2D for 4.0+3.0 years (HbA1c 7.5± 0.5% on metformin alone) in auxiliary research to the Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE). T-cell autoreactivity against islet proteins, islet autoantibodies against the 65-kDa GAD antigen, IA-2, zinc transporter-8, and -cell function were all assessed. About 41.3% had cellular islet autoimmune, 13.5% had humoral islet autoimmunity, and 5.3% had both.
β-Cell function (iAUC-CG) and C-peptide(0–30)/glucose(0–30) from an oral glucose tolerance test were lower in T-cell–positive (T+) than T-cell–negative (T) individuals using two different insulin sensitivity adjustments (iAUC-CG: 13.2% [95% CI 0.3, 24.4] or 11.4% [95% CI 0.4, 21.2] lower; C-peptide [0–30 T+ patients had 17.7% higher HbA1c (95% CI 0.07, 0.28) and 7.7% higher fasting plasma glucose levels (95% CI 0.2, 15.3) than T patients. Researchers concluded that islet autoimmunity in T2D patients is substantially more common than previously thought. T-cell autoimmunity was linked to decreased -cell function and poor glucose management.