Aims: To study the impact of genetic factor on pancreatic beta-cell function in the Chinese population.
Methods: 233 first-degree relatives of patients with type 2 diabetes (T2D) with no history of blood glucose abnormalities and their 190 spouses, who did not have a family history of T2D, underwent a 75-g oral glucose tolerance test (OGTT). Based upon the OGTT, these two groups were further divided into three subgroups, including groups with normal glucose tolerance (NGT), impaired glucose regulation (IGR), and type 2 diabetes. Insulin resistance (IR) was evaluated using the homeostasis model assessment-IR (HOMA-IR), beta-cell function indices of basal and first-phase were measured by DI1 (HOMA-beta/HOMA-IR) and DI2 (DeltaI30/DeltaG30/HOMA-IR), respectively.
Results: Among the first-degree relatives and their spouses, the HOMA-IR was highest in the T2D group and lowest in the NGT group. However, the HOMA-beta, DI1 and DI2 declined significantly with progressive reductions in glucose tolerance (P<0.01 or 0.05). DI1 and DI2 of the NGT group of first-degree relatives (FNGT) were significantly lower than those of the spouse NGT (SNGT) group (P<0.05). DI1 and DI2 of the IGR of first-degree relatives (FIGR) group were significantly lower than those of the spouse IGR (SIGR) group.
Conclusions: Defects in pancreatic beta-cell function exist in the first-degree relatives, who have different glucose tolerance statuses, of T2D patients. These defects are more profound in FNGT and FIGR when compared to their spouses in corresponding glucose tolerance subgroups. However, there is no difference in IR between the corresponding glucose tolerance subgroups of the first-degree relatives and their spouses. It suggests that the genetic factor possibly aggravates beta-cell lesion.