For other clinical features, the strongest evidence was that, in many observational studies, markers of lower insulin secretion (including longer diabetes duration [or proxies such as insulin treatment], lower fasting C-peptide, lower urine C-peptide-to-creatinine ratio, and positive glutamic acid decarboxylase (GAD) or islet antigen 2 (IA2) islet autoantibodies) were associated with lesser glycaemic response to GLP1-RA36–49. This evidence concerns the gene GLP1R and diabetes mellitus.