Explore the occurrence and development of β cell dysfunction and insulin resistance according to the stratification on normal glucose tolerance / 中华内分泌代谢杂志

ABSTRACT

After the stratification of the normal glucose tolerance, the changes of insulin resistance and βcell function in the development of type 2 diabetes mellitus were investigated. A retrospective analysis on data of 275 cases with oral glucose insulin releasing tests. The area under the insulin curve (AUCINS ) 108. 43 mU/ L was taken as the critical value of diagnosis. Normal glucose tolerance subjects were divided into the NGT-a group(AUCINS<108. 43 mU/ L) and the NGT-b group(AUCINS≥108. 43 mU/ L). The plasma glucose, insulin, insulin sensitivity, and β cell function were compared among the 4 groups NGT-a group (n=96), NGT-b group (n=49), prediabetes group (n=71), and type 2 diabetes mellitus group ( n = 59). Among the fasting insulin, 2 h insulin, AUCINS , early-phase insulin secretion index(△I30 / △G30), the ratio of total insulin area under curve, and total glucose area under curve, disposition index, homeostasis model assessment for insulin resistance, and Matsuda insulin sensitivity index, the relationship as follows NGT-b group>prediabetes group>NGT-a group>type 2 diabetes mellitus group. The NGT-b group was always the highest, prediabetes group was lower, NGT-a group and type 2 diabetes mellitus group were the lowest, there were significant differences (all P<0. 05). Making the NGT-a group as the basic state, in the NGT-b group, β cell function has begun to appear compensation and insulin resistance, and β cell function compensation reached the peak, the β cell function in the prediabetes group was beginning to compensate for the deficiency, the function of β cell in type 2 diabetes mellitus group decreased further. These findings suggest that the development process of type 2 diabetes mellitus could be the following four stages according to the function of β cell β cell function normal, β cell functional compensation, β cell function loss of compensation, and finally β cell function failure.