Before the manifestation of the metabolic defects that lead to type 2 diabetes, fasting and postprandial insulin levels are similar and constant. In the majority of patients in whom type 2 diabetes develops, increasing insulin resistance leads to compensatory increases in circulating insulin, which prevents an increase in glucose levels.
As time progresses, the insulin resistance reaches a peak and stabilizes, while the compensatory increase in insulin continues to prevent fasting glucose levels from becoming abnormal.
However, at some point, either because of early beta-cell dysfunction or because of a natural limit of beta-cell capacity, challenge of this delicate balance with a glucose load may demonstrate that, although fasting glucose levels remain normal, postprandial glucose levels become abnormal as a limitation in insulin response is reached.
Following the onset of beta-cell dysfunction, insulin levels can no longer keep up in overcoming the insulin resistance, and fasting and postprandial glucose levels increase progressively over time.