Insulin, a principal anabolic hormone produced by pancreatic b-cells, has a primary function of storage of nutrients following excessive energy intake. Pre- or early type 2 diabetes stages present hyperinsulinemia (b-cell dysfunction) and insulin resistance. Initiation of hyperinsulinemia is triggered by a loss of first-phase glucose-stimulated insulin secretion with altered membrane ion channel distribution. More factors, including insulin resistance and excessive proliferation of b-cells, deteriorate the hyperinsulinemia, whereas the hyperinsulinemia contributes to further development of insulin resistance and type 2 diabetes; to develop eventually late-stage diabetes with absolute insulin deficiency. In this mini-review, the major focus was put on the causes and pathophysiology of hyperinsulinemia, and the metabolic consequences and current treatment of hyperinsulinemia were discussed. The data used in this narrative review were collected mainly from relevant discoveries in the past 3 years.