Description: The last decade has witnessed a remarkable progress in the elucidation of cell mechanisms of insulin resistance (IR), as well as in its importance for the appearance and maintenance of hyperglycaemia that accompanies type 2 diabetes mellitus (T2DM). At the same time, the role of impaired beta-cell function for the development of T2DM remains insufficiently researched. That is why, the purpose of this review was to provide and analyse information about the role and significance of reduced functional activity of beta-cells for T2DM onset and the pathogenetic mechanisms of impaired insulin secretion. The data presented clearly suggest that the transition of impaired glucose tolerance into overt diabetes absolutely requires a disturbance in beta-cell function, resp. insulin secretion. Regardless of the numerous unclear issues about the mechanisms of beta-cell dysfunction, it could be claimed that many factors provoking IR (obesity, increased free fatty acid concentrations, increased levels of some adipokines, free radicals etc.) results in disturbance of beta-cell functional activity. The increased amyloid deposition in the pancreas is not less important. The currently prevailing opinion is that while IR is rather a consequence of adverse environmental effects, the beta-cell impairment is geneнtiнcally determined. Therefore, the risk of T2DM development increases extremely when genetic predisнposition to impaired beta-cell function is combined with harmful environmental effects resulting in IR development