What are the characteristics of phenotypic type 2 diabetic patients with low-titer GAD65 antibodies?

Type 2 diabetes results from combined insulin resistance and beta-cell deficiency. Type 1 diabetes results from beta-cell destruction associated with islet autoantibodies, including those directed against glutamate decarboxylase (GAD(65) antibodies [GADA]). Clinical impact of low GADA positivity (< 60 U/ml) in type 2 diabetes is debated, being rarely performed in routine care. The aim of our study was to determine the prevalence and cardiometabolic/autoimmune phenotype of GADA[+] patients. 524 type 2 diabetes consecutive outpatients were assessed for glucose homeostasis using homeostasis model assessment (HOMA): insulin sensitivity (HOMA S); beta-cell function (HOMA B) and annualized loss in [BXS]. GADA prevalence was 6 % (n = 30). There were no differences between groups for age, diabetes duration and family history of diabetes. There were proportionately more women (33 vs. 53 %) in GADA[+]. There were no differences in body mass index, waist circumference or visceral fat. HOMA S was lower than normal, with no difference between groups, as was HOMA B. Annualized rate of [BXS] loss was 1.26 %/year (GADA[+]) versus 1.34 %/year (GADA[-]; NS). HbA1c was 7.8 % (GADA[+]) versus 7.6 % (GADA[-]; NS). Among all patients, prevalence of autoimmune thyroid disease was 10 %. In GADA[+], this prevalence was significantly increased and equally affected both sexes: 29 % (men) versus 25 % (women), while for GADA[-] the prevalence was 5 % (men) versus 18 % (women; p < 0.0001). Low-titer GADA autoimmunity among type 2 diabetes patients was not associated with accelerated beta-cell function, nor with any distinctive cardiometabolic phenotype, but for a markedly increased prevalence of autoimmune thyroid disease, especially among men.