(HealthDay News) — In patients with type 2 diabetes, characteristics and biomarkers of beta-cell failure are associated with glycemic response to glucagon-like peptide-1 (GLP-1) receptor agonist therapy, according to a study published in Diabetes Care.
Angus G. Jones, MBBS, from the University of Exeter Medical School in the United Kingdom, and colleagues examined whether clinical characteristics and simple biomarkers of beta-cell failure correlate with individual variation in glycemic response to GLP-1 receptor agonist therapy.
Six hundred twenty participants with type 2 diabetes and HbA1c of 7.5% or greater commencing GLP-1 receptor agonist therapy were studied prospectively and their response to therapy was assessed over 6 months.
The researchers observed a correlation between reduced glycemic response to GLP-1 receptor agonists and longer duration diabetes, insulin cotreatment, lower fasting C-peptide, lower post-meal urine C-peptide-to-creatinine ratio and positive GAD or IA2 islet autoantibodies (all P≤.01).
Markedly reduced glycemic response to GLP-1 receptor agonist therapy was seen for participants with positive autoantibodies (mean HbA1c change, −0.5% vs. −1.4%; P=.005) or severe insulin deficiency (C-peptide <0.25 nmol/L, mean change −0.2% vs. −1.4%; P=.002). These markers were mainly seen in insulin-treated participants and did not correlate with weight change.
“Clinical markers of low beta-cell function are associated with reduced glycemic response to [GLP-1 receptor agonist] therapy,” the researchers wrote. “C-peptide and islet autoantibodies represent potential biomarkers for the stratification of GLP-1RA therapy in insulin-treated diabetes.”