A family history of diabetes (FHD), especially in both parents, impairs residual β-cell function in type 2 diabetes (T2D) patients, a new study has shown.
Researchers enrolled 1,131 T2D patients who were then grouped according to FHD: without FHD (FHD–; n=559; mean age, 65.8±11.3 years; 63.5 percent male); those with at least one sibling, but no parent, who had diabetes (FHD+; n=151; mean age, 69.1±9.5 years; 48.3 percent male); and those with one (FHD++; n=385; mean age, 61.2±12.2 years; 63.4 percent male) or both (FHD+++; n=36; mean age, 62.0±11.4 years; 55.6 percent male) parents with diabetes. Clinical features were compared across patient groups.
Patients in the FHD+++ group were diagnosed with diabetes at the youngest age (p<0.001). They also had the lowest levels of insulin secretion (p<0.01) and the highest percentage of insulin requirement (p<0.05).
Moreover, in all groups positive for an FHD, β-cell function-related parameters showed an inverse correlation with insulin secretory capacity. This was particularly evident in the FHD+++ group (β for fasting serum C-peptide immunoreactivity [F-CPR], –0.12; p<0.01; β for CPR index [CPI], –0.11; p<0.05).
F-CPR was measured using electochemiluminescence immunoassays and the generated values were used for the calculation of CPI. These figures were used for the assessment of residual pancreatic β-cell function.
“[W]e have demonstrated that the degree in the association of FHD with residual β-cell function differs according to the number and type of FHD. This finding may partly account for the heterogeneous progression in β-cell dysfunction among individual T2D patients that is seen after the onset of the disease,” the researchers said.