Nature of beta-cell failure tied to glycemic response to GLP-1RA
(HealthDay)—In patients with type 2 diabetes, characteristics and biomarkers of β-cell failure are associated with glycemic response to GLP-1 receptor agonist (GLP-1RA) therapy, according to a study published online Aug. 4 in Diabetes Care.
Angus G. Jones, M.B.B.S., from the University of Exeter Medical School in the United Kingdom, and colleagues examined whether clinical characteristics and simple biomarkers of β-cell failure correlate with individual variation in glycemic response to GLP-1RA therapy. Six hundred twenty participants with type 2 diabetes and hemoglobin A1c (HbA1c) ≥7.5 percent commencing GLP-1RA therapy were studied prospectively and their response to therapy was assessed over six months.
The researchers observed a correlation between reduced glycemic response to GLP-1RAs 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 ≤ 0.01). Markedly reduced glycemic response to GLP-1RA therapy was seen for participants with positive autoantibodies (mean HbA1c change, −0.5 versus −1.4 percent; P = 0.005) or severe insulin deficiency (C-peptide <0.25 nmol/L, mean change −0.2 versus −1.4 percent; P = 0.002). These markers were mainly seen in insulin-treated participants and did not correlate with weight change.
"Clinical markers of low β-cell function are associated with reduced glycemic response to GLP-1RA therapy," the authors write. "C-peptide and islet autoantibodies represent potential biomarkers for the stratification of GLP-1RA therapy in insulin-treated diabetes."
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